Transcript Nervous System Infections - Biology Online Learning

Nervous System and Blood
Infections
Meningococcal Meningitis
• Symptoms
• First symptoms similar
regardless of agent
• Mild cold followed by
onset of throbbing
headache
• Fever
• Pain and stiffness of neck
and back
• Nausea and vomiting
• Deafness and alteration in
consciousness may appear
progressing to coma
• Small hemorrhages called
petechiae may appear on skin
• Infected person may develop
shock and die within 24 hours
• Usually progression of disease
is slower allowing time for
treatment
Meningococcal Meningitis
• Pathogenesis
• Acquired by inhaling
infected respiratory
droplets
• Bacteria adhere to
mucous membranes via
pili and multiply
• Invade bloodstream by
passing through
respiratory epithelium
• Bloodstream carries
organisms to CSF
• Organisms phagocytized
by PMNs
• Enter fluid in large
numbers
• Inflammation causes swelling
and infarcts to brain tissue
• Can also cause obstruction of
outflow of CSF
• Causes brain to squeeze
against skull
• Release of endotoxin causes
drop in blood pressure leading to
shock
Meningococcal Meningitis
• Causative agent
• Neisseria meningitids
• Gram negative
diplococci
• 12 antigenic serotypes
• Most serious
infections due to
types A,B,C and Y
• Epidemiology
• N. meningitis more prone to
cause epidemics
• Reasons unknown
• Can spread rapidly in
crowded stressed places
• Human only source of
infection
• Transmission can occur with
disease or asymptomatic
carrier
• Organism recovered from 5% 15% of healthy individuals
Meningococcal Meningitis
• Prevention and Treatment
• Vaccine is available
• Used to control epidemics
• Not given routinely due to ineffectiveness in children less than
2 years of age
• Effect is not long lasting
• Mass prophylaxis with antibiotics helpful at controlling
epidemics in small populations
• Individuals immediately exposed given antibiotic
rifampin
• Can usually be cured unless brain injury or shock
present
• Mortality is less than 10% in treated populations
Listeriosis
• Symptoms
• Most cases asymptomatic
• Symptoms include
• Fever and muscle aches
• Sometimes nausea and diarrhea
• 75% of cases coming to medical attention have
meningitis
• With typical symptoms of meningitis
• Pregnant women who become infected often
miscarry or deliver terminally ill infants
Listeriosis
• Causative agent
• Listeria monocytogenes
• Motile, non-spore forming, facultative Gram (+) rod
• Pathogenesis
• Mode of entry usually obscure
• Generally thought to enter through GI tract
• Bacteria penetrate intestinal mucosa then enter the
bloodstream
• Leads to bacteriemia
• Organism can cross the placenta
• Produces abscesses in fetal tissues
• Babies usually develop meningitis after 1-4 week incubation
period
Listeriosis
• Epidemiology
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Widespread in natural waters and vegetation
Can be carried asymptomatically in animals and humans
Occurs on all continents except Antarctica
Pregnant women, elderly and immuncompromised at
highest risk
• Advised to refrain from soft cheeses and reheat leftovers
• Epidemics have resulted from contaminated foods
• Organism can survive in commercially prepared foods and at
refrigeration temperatures
Hansen’s Disease (leprosy)
• Symptoms
• Begins gradually
• Usually with onset of increased or
decreased sensation in certain areas of
skin
• These areas usually have changes in
pigmentation
• Affected areas later enlarge and thicken
• Loss of hair, ability to sweat and
sensation
• Nerves in extremities visibly enlarge
• Usually accompanied with pain that
proceeds to numbness, muscle wasting,
ulceration
• Loss of fingers and toes follows
• Changes most obvious in face
• Thickening of nose and ears with deep
wrinkling
Hansen’s Disease (leprosy)
• Causative agent
• Mycobacterium leprae
• Aerobic, acid-fast, rod
shaped
• Grows slowly
• Generation time
approximately 12 days
Hansen’s Disease (leprosy)
• Pathogenesis
• Earliest detectable findings in humans is infection of small nerves of
skin
• Generally via biopsy of skin lesion
• Only know human pathogen to preferentially attack peripheral
nerves
• Grows slowly within macrophages
• Course of infection depends on immune response
• Macrophages limit growth of organism
• Disease may spontaneously stop progressing
• Nerve damage although permanent doesn’t progress
• Tuberculoid leprosy
• Rarely transmitted to others
• Uncommon form termed lepromatous leprosy
• High numbers of bacteria mucous membranes with very little
inflammation
Hansen’s Disease (leprosy)
• Epidemiology
• Transmission via direct
human-to-human contact
• Disease develops in
small number of people
• Controlled by body
defenses
• Natural infections occur
in wild nine banded
armadillos and
mangabey monkeys
• Armadillos not a
source of human
infection
• Prevention and Treatment
• No proven vaccine
• Dapsone and rifampin used to
arrest tuberculoid leprosy
• Treated for 6 months
• Lepromatous treated for 2
years
• Combination therapy required
to control resistance
Botulism
• Symptoms
• Begins 12 to 36 hours post ingestions of
contaminated foods
• Begins with dizziness, dry mouth and blurred
vision
• Abdominal symptoms include pain, nausea,
vomiting and diarrhea or constipation
• Progressive paralysis ensues
• Paralysis of respiratory muscles most common
cause of death
• Paralysis distinguishes botulism from other forms
of food poisoning
Botulism
• Causative agent
• Clostridium botulinum
• Gram (+), spore forming rod
shaped
• Endospores generally
resist boiling for hours
• Killed by autoclaving
• Produces toxin
• 7 different toxins
• A, B, C1, D, E, F, G
• All produced by
different strains
• A, B, E, F responsible for
most human cases
Botulism
• Pathogenesis
• Spores germinate in favorable environment
• Bacterial growth results in toxin release
• Toxin resist digestion and is absorbed by small intestine
• Toxin can circulate in blood stream for 3 weeks or more
• Toxin is neurotoxin
• Acts against nervous system
• One of most powerful poisons known
• Toxin attaches to motor nerves blocking function of
neurotransmitter
• Causes paralysis
• Toxin is AB toxin
• B portion binds and A portion enters nerve cell
Botulism
• Epidemiology
• Widely distributed in soils and aquatic
sediments
• In early 20th century foodborne outbreaks
common
• Strict controls on commercially canned foods
decreases incidence
Botulism
• Intestinal botulism
more common than
foodborne
• Intestinal occurs in
small children to 6
months of age
• Results in mild disease
ranging from mild
lethargy to respiratory
insufficiency.
• Flaccid Baby Syndrome
Botulism
• Prevention and Treatment
• Prevention depends on proper sterilization and sealing
of canned food
• Heating food to 100°C for 15 minutes just prior to
eating generally makes food safe to eat
• Can’t rely on smell, taste or appearance to detect
contamination
• Treated by intravenous administration of antitoxin
ASAP
• Antitoxin only neutralizes circulating toxin
• Affected nerves recover slowly
• Gastric washing and surgical removal of tissues
removes unabsorbed toxin
• Artificial respiration may be required for prolonged
periods
Viral Meningitis
• Symptoms
• Typically abrupt in onset
• Characterized by
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Fever
Severe headache above or behind eyes
Stiff neck with increased pain on forward flexion
Sensitivity to light
Nausea and vomiting
May have sore throat, chest pain, swollen parotid
gland and skin rash
• Depends on causative agent
Viral Meningitis
• Causative agent
• Small, non-enveloped
RNA virus
• Member of the
enterovirus subgroup
of picornavirus family
• Responsible for at least
half of viral meningitis
cases
• Most common
offenders are coxsackie
virus and echovirus
• Pathogenesis
• Begins with infection of
throat and intestinal
epithelium
• Progresses to lymphoid
tissue in the bloodstream
• Viremia results in
meningeal infection
• May also be responsible for
rash and chest pain
Viral Meningitis
• Epidemiology
• Relatively stable in
environment
• Can survive in
chlorinated water
• Infected often
eliminate virus in
feces
• Often for weeks
• Transmission via
fecal-oral route
• Mumps virus
transmitted via
respiratory droplets
• Prevention and
Treatment
• Handwashing and
avoidance of crowded
swimming pools
• When aseptic disease
present in community
• No vaccine against
coxsakievirus and
echoviruses
• Mumps virus controlled
via immunization
Viral Encephalitis
• Symptoms
• Onset usually abrupt
• Characterized by
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fever
Headache
Vomiting
one or more nervous system abnormalities
• Disorientation, localized paralysis, deafness, seizures or
coma
Viral Encephalitis
• Causative agent
• Arboviruses
• Arthropod borne viruses
• Transmitted by insects,
mites and ticks
• Viruses enveloped
single stranded RNA
viruses
Viral Encephalitis
• Pathogenesis
• Knowledge of pathogenesis incomplete
• Viruses multiply at site of bite and in local lymph nodes
• Produces viremia
• Virus crosses blood-brain barrier
• Mechanism unknown
• Causes extensive damage to brain tissue in severe cases
• Progression of disease halted with appearance of
neutralizing antibody
• Mortality ranges from 2% to 50% depending of type of
infecting agent
• Disabilities often present in those who recover
Viral Encephalitis
• Epidemiology
• Only minority infected develop encephalitis
• Other develop viral meningitis
• Disease are all zoonoses
• Maintained naturally in birds and rodents
• Humans are accidental hosts
• LaCrosse encephalitis usually causes most
cases of encephalitis
Viral Encephalitis
• Prevention and Treatment
• Animals often used to identify emergence of disease
• Equine encephalitis generally infects horses 1 – 2 weeks
before first human case seen
• Sentinel chickens serve same function
• Prevention directed towards
• Avoiding outdoor activities at night when mosquito
populations highest
• Make sure windows and porches properly screened
• Use insect repellents and insecticides
• No proven antiviral therapy
Infantile Paralysis, Polio
• Symptoms
• Usually begins with symptoms
of meningitis
• Pain and spasm of muscles
generally occur
• This is usually followed by
paralysis
• Paralyzed muscles shrink and
bones do not form normally
• In severe cases respiratory
muscles become paralyzed
• Artificial respiration is required
• Some recovery if patient
survives acute stage
Infantile Paralysis, Polio
• Causative agent
• Poliovirus
• There are three types
• 1, 2 and 3
• Distinguished
via anitsera
• Small, enveloped,
single-stranded RNA
virus
• Member of picornavirus
• Subgroup enterovirus
Infantile Paralysis, Polio
• Pathogenesis
• Enter body orally
• Virus infects the throat and
intestinal tract
• Then moves to bloodstream
• Immune system conquers
infection in most people
• Viruses enters nervous system
of small percentage of people
• Virus attacks motor nerves
• Infected cells are destroyed upon
cell release
• Post-polio syndrome
• Development of muscle
weakness and pain many years
after acute disease
Infantile Paralysis, Polio
• Epidemiology
• Virus widespread in areas where sanitation is
poor
• Virus usually spread via fecal-oral route
• In endemic areas people generally do not
escape childhood without contracting disease
• These individuals develop immunity
• Babies receive antibodies transplacentally
• Babies develop disease within 2 to 3 months of age
• Develop lifelong immunity
Infantile Paralysis, Polio
• Prevention and Treatment
• Virus stable under natural conditions
• Inactivated by pasteurization and chlorination
• Control directed at vaccination
• Oral vaccine until 1999
• Vaccine cause of some cases of polio
• Oral vaccine discontinued
• New injectable vaccine introduced in 1999
Rabies
• Symptoms
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Fever
Head and muscle ache
Sore throat
Fatigue
Nausea
Tingling or twitching
at site of viral entry
• Characteristic symptom
• Early symptoms begin 1 to 2
months post infection
• Progress rapidly to secondary
symptoms of
• Encephalitis, agitation,
confusion, hallucinations,
seizure, increased sensitivity
to light and touch
• Body temperature rises with
increased salivation and
difficulty swallowing
• Results in frothing of mouth
• Hydrophobia occurs in 50% of
cases
• Coma develops
• About 50% of patients die
within 4 days
Rabies
• Causative agent
• Rabies virus
• Member of rhabdovirus family
• Sticking bullet shape
• Enveloped, single-stranded RNA genome
• Pathogenesis
• Mode of transmission primarily via saliva
of rabid animal
• Usually due to bite or abrasion
• Can be contacted via inhalation
• Virus multiples in muscle cells at site of
infection
• Virus reaches brain via infected nerve
• Virus multiplies extensively in brain
• Negri bodies form at sites of replication
Rabies
• Epidemiology
• Widespread in wild animals
• 5,000 cases reported annually in
United States
• Skunks, raccoons and bats
considered chief reservoir
• Raccoons most infected
• Almost all human cases due to
contact with infected bats
• Zero to 4 reported cases in U.S
annually
• Only 25% have history of dog
bite
• Long incubation period of virus
make history unreliable
Rabies
• Prevention and Treatment
• Wash wound immediately and thoroughly
• Use soap and water and apply antiseptic
• Risk of developing rabies from bite of rabid dog is
approximately 30%
• Risk can be lowered considerably if vaccine is administered as
soon as possible after exposure
• Presumably vaccine provokes better immune response
• Bitten individual should receive series of 5 injections at
wound site and intramuscularly
• Shots should be given even if biting animal presumed to be
rabid
• No effective treatment for rabies
• Only six know survivors of disease
Cryptococcal Meningioencephalitis
• Symptoms
• Develop gradually in healthy individuals
• Generally consist of
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Difficulty thinking
Dizziness
Intermittent headache
Slight or no fever
• Slow progression of disease results in other symptoms
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Vomiting
Weight loss
Paralysis
Seizures
coma
Cryptococcal Meningioencephalitis
• Causative agent
• Yeast form of Filobasidiella
neoformans fungus
• Small, spherical yeast
• Generally surrounded by large
capsule
Cryptococcal Meningioencephalitis
• Pathogenesis
• Fungus becomes airborne in dust
• Enters body via inhalation and establishes infection first in
lung
• Infection often eliminated by body defenses
• Organism multiplies and enters bloodstream
• Capsule inhibits phagocytosis and neutralizes opsonins
• Organisms typically cause thickening of meninges
• This can often impede the flow of CSF
• Also invade brain tissue producing abscesses
Cryptococcal Meningioencephalitis
• Epidemiology
• Distributed worldwide in soil and vegetation
• Numerous in soil where pigeon droppings
accumulate
• For every one case of disease millions are
infected with organism
• Symptomatic infection often the first indicator
of AIDS
• Person-to-person spread does not occur
Cryptococcal Meningioencephalitis
• Prevention and Treatment
• No vaccine or other preventative measures
• Treatment with amphotericin B is effective
• Often given concurrently with flucytosine or
itraconazole
• Amphotericin B does not reliably cross blood-brain
barrier
• Drug administered through tube inserted through the skull
into lateral ventricle
African Sleeping Sickness
• Symptoms
• First symptoms appear within a week after bite from
tsetse fly
• Nodule develops at site of bite
• Regional lymph nodes enlarge
• Symptoms may disappear spontaneously
• Weeks or years later recurrent fevers develop
• CNS involvement marked by gradual loss of interest in
everything
• Marked by decreased activity and indifference to food
• Eyelids droop and individual falls asleep during
everyday tasks
• Speech becomes slurred followed by coma and death
African Sleeping Sickness
• Causative agent
• Trypanosoma brucei
• Flagellated protozoan
• Slender with wavy undulating
membrane
• Two subspecies
• T. brucei rhodesiense
• Occurs mainly in cattleraising areas of East Africa
• T. brucei gambiense
• Occurs mainly in forested
areas of Central and West
Africa
• Transmitted by tsetse fly
African Sleeping Sickness
• Pathogenesis
• Protozoan enters through bite in fly saliva
• Organism multiplies at skin and migrates to lymphatic
and blood circulation
• Body responds with fever and IgM antibody
• Symptoms improve
• Period followed by recurrent increases in numbers of
parasite
• Termed parasitemica
• Parasitemia and antibody production continue until treatment or
death
• T. brucei rhodesiense infections progress quickly often
with major system involvement with 6 weeks and death
in 6 months
• T. brucei gambiense infections progress much more
slowly
African Sleeping Sickness
• Epidemiology
• Disease occurs on African continent within 15°
of equator
• 10,000 to 20,000 new cases annually
• Occurrence of disease is determined by
distribution of tsetse fly
• Wild animals main reservoir for Rhodesian form
• Humans are main reservoir for Gambian form
• Human-to-human transmission more common
African Sleeping Sickness
• Prevention and Treatment
• Prevention measures directed against tsetse fly vectors
include
• Insect repellents and protective clothing
• Traps with bait and insecticide
• Clearing brush
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Treatment of infected individuals help reduce reservoir
Single injection of pentamidine prevents Gambian form
Suramin can be used if no CNS involvement
Melarsoprol and eflornithine used with CNS
involvement
Transmissible Spongiform
Encephalopathies
• Symptoms
• Early symptoms
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Vague behavioral changes
Anxiety
Insomnia
Fatigue
• These symptoms progress weeks to months to hallmark
symptoms
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Muscle jerks
Lack of coordination
Dementia
Deteriorating intellectual function
Impaired judgment
Memory loss
• Disease often progresses to death within a year
Transmissible Spongiform
Encephalopathies
• Causative agent
• Proteinaceous infectious particles
• a.k.a prions
• Appear to be new class of infectious agent
• Differ from bacteria, viruses and viroids
• Main characteristics
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Increase in quantity during incubation period
Resist inactivation via UV and ionizing radiation
Resist inactivation by formaldehyde and heat
Not readily destroyed by proteases
Not destroyed by nucleases
Much smaller than smallest virus
Composed of protein coded by normal cellular gene
• Modified after transcription
Transmissible Spongiform
Encephalopathies
• Pathogenesis
• No inflammatory or immune response produced
• Replication depends on presence of normal
cellular protein
• Replicate by converting normal protein into copies of
themselves
• Normal course of infections
• Replication in spleen
• Most likely in dendritic cells
• Then transported to nervous system via nerve axon
• Prions aggregate in insoluble masses in nerve cells
• Causes malfunction and death
Transmissible Spongiform
Encephalopathies
• Epidemiology
• Creutzfeld-Jakob occurs in humans over age 45
• Human-to-human transmission has occurred via corneal
transplants
• Scrapie found in sheep
• Most likely transmitted from ewe to lamb
• Mad cow disease result of cattle exposed to scrapie in
cattle feed
• New varient Creutzfeld-Jakob mostly likely due to
exposure of human to mad cow disease
• Median age of onset of NVCJ is 28 years
Transmissible Spongiform
Encephalopathies
• Prevention and Treatment
• Prions inactivated by autoclaving in 1N NaOH
• No treatment
• All forms are fatal
Subacute Bacterial Endocarditis
• Symptoms
• Marked fatigue and slight fever
• Typically become ill gradually
• Slowly lose energy over a period of weeks or months
• Abrupt development of stroke may occur
• Causative Agent
• Usually member of normal bacterial flora of
mouth and skin
• α-hemolytic viridians streptococci and
Staphylococcus epidermis
Subacute Bacterial Endocarditis
• Pathogenesis
• Bacteria gain entry to bloodstream during dental
procedures, toothbrushing or other trauma to mouth or
skin
• Organisms may become trapped in clots formed near
deformed heart valves
• Organism may multiply and produce biofilms
• Organisms inaccessible to phagocytic killing
• As organisms multiply more clot is formed
• Clot builds to fragile mass
• Bacteria break away from clot and are washed away
• Clots may block significant vessels
• Leads to tissue death, infarction and aneurysm
• Masses of organism growing in heart can burrow into
tissue and cause abscesses
Subacute Bacterial Endocarditis
• Epidemiology
• Viridians streptococci account for smaller
portion of cases
• Due to dentist prescribing antibiotics to patients with
distinct heart murmurs before treatment
• More cases of disease produced by
Staphylococcus epidermidis
• Occur most often in
• Injected-drug users
• Patients with intravenous catheter
• Particularly if used for extended periods
• Individuals with artificial heart valves
Subacute Bacterial Endocarditis
• Prevention and Treatment
• No proven prevention
• Antimicrobial treatment to susceptible population
previous to dental procedures most notable attempt to
prevent
• Rigid attention to sterile technique helps prevent
occurrence in hospital setting
• Only bacteriocidal medication are effective in
treatment
• Usually two or more given together for prolonged
period
• Penicillin and gentimicin given over one or more months
Gram Negative Septicemia
• Symptoms
• Violent shaking chills and fever
• Often accompanied by anxiety and rapid breathing
• In case of septic shock
• Urine output drops
• Respiration and pulse become more rapid
• Arms and legs become cool and dusky colored
Subacute Bacterial Endocarditis
• Causative agent
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Gram (-) bacteria more likely cause of fatal septicemia
Shock is common despite treatment
Mortality rate nearly 50%
Blood cultures from patients usually reveal
• E. coli
• Gram (-) facultative anaerobe
• Ps. Aeruginosa
• Gram (-) aerobe
• Generally found in natural environment
• Bacteroides sp.
• Gram (-) aerobe
• Part of normal intestinal and upper respiratory flora
Subacute Bacterial Endocarditis
• Pathogenesis
• Generally originates outside of
bloodstream
• Alterations in normal body defenses may
allow organism to infect blood
• Endotoxin is released
• Antibiotics can enhance endotoxin release
• Macrophages respond intensely to
endotoxin to try to localize
• Exaggerated response considered
hypersensitivity
• Failed localization allows endotoxin into
bloodstream
• Causes cascade of harmful events
• Lungs particularly susceptible to
irreversible damage
• Often results in death despite successful
treatment of infection
Subacute Bacterial Endocarditis
• Epidemiology
• Mainly a nosocomial disease
• Reflects high incidence of Gram (-) bacteriemia in
hospitals
• General trend to increasing disease that relates
to increased life span, antibiotic suppression of
normal flora, use of immunosuppressive drugs
and biofilm formation of medical devices
Subacute Bacterial Endocarditis
• Prevention and Treatment
• Depends largely on identification and effective
treatment of localized infections
• Treatment against causative organisms
• Treatment methods will vary according to infecting
organism
Tularemia (Rabbit Fever)
• Symptoms
• Characterized by
development of skin
ulcerations and
enlargement of
regional lymph nodes
• Other symptoms
include
• Fever
• Chills
• Achiness
• Symptoms usually abate
in 1 to 4 weeks
• Sometimes may become
chronic
• Mortality rate between
30% and 50%
Tularemia (Rabbit Fever)
• Causative agent
• Francisella tularensis
• Non-motile, aerobic, Gram (-) rod
• Pathogenesis
• Causes ulcer at entry sight
• Lymphatic vessels carry organism to regional lymph nodes
• Become large, tender and filled with pus
• Spread to other body sites via lymphatics and blood vessels
• Pneumonia occurs in 10% -15% of lung infections
• Mortality rate as high as 30%
• Multiplies within phagocytes
• Cell mediated immunity responsible for ridding infection
• 90% of infected individuals survive in the absence of treatment
Tularemia (Rabbit Fever)
• Epidemiology
• Occurs among wild animals in Northern
Hemisphere
• In eastern U.S. most infections occur in winter
• Result from skinning hunted rabbits
• In western U.S. infections increase in summer
• Due to bites from fleas and ticks
• Other reservoirs for infection include
• Muskrats, beavers, squirrels, and deer
• Animals generally free of illness
Tularemia (Rabbit Fever)
• Prevention and Treatment
• Uses of Rubber gloves and goggles when
working with animal carcasses
• Insect repellents and protective clothing
• Inspect routinely for ticks after exposure
• Vaccine available for workers at higher risk of
exposure
• Treated with gentimicin
Brucellosis (Undulant Fever)
• Symptoms
• Onset usually gradual and symptoms vague
• Symptoms include
• Aches and pains
• Enlarged lymph nodes
• Weight loss
• Without treatment most cases recover within 2
months
• 15% will be symptomatic for 3 months or longer
Brucellosis (Undulant Fever)
• Causative agent
• Four varieties of genus Brucella cause disease
in humans
• All fall into a single species Brucella melitensis
• Traditionally each variety given own species name
depending on preferred host
• B. abortus  cattle
• B. canis  dogs
• B. melitensis  goats
• B. suis  pigs
• Organism is Gram (-) rod
Brucellosis (Undulant Fever)
• Pathogenesis
• Organism penetrates mucous membranes or break in
skin
• Disseminated via lymphatic or blood vessels
• Generally to heart and kidneys
• Spleen enlarges in response to infection
• Organisms resistant to phagocytic killing
• Can grow within phagocytes
• These organisms inaccessible to antibodies and some
antibiotics
• Mortality generally due to endocarditis
• Rate is approximately 2%
• Osteomyelitis is often serious side effect
Brucellosis (Undulant Fever)
• Epidemiology
• Chronic infection of domestic animals
• Generally involving the mammary gland and uterus
• Causes contaminated milk and abortions
• Abortion not a feature of human disease
• Occurs in workers in meat packing industry
• Major problem in animals used for food
Brucellosis (Undulant Fever)
• Prevention and Treatment
• Pasteurization most important control measure
• Inspection of domestic animals
• Protective eyewear and gloves when working
with animals or animal carcass
• Attenuated vaccine controls disease in domestic
animals
• Tetracycline combined with rifampin used for
treatment
• Treatment usually given for 6 weeks
Plague (Black Death)
• Symptoms
• Develop abruptly 1 – 6 days post infection
• Transmission via bite from infected flea
• Disease characterized by large tender lymph nodes called
buboes
• Other symptoms include
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High fever
Shock
Delirium
Patchy bleeding under the skin
May also have cough and bloody sputum
• Only in lungs infected
• Pneumonic plague
Plague (Black Death)
• Causative agent
• Yersinia pestis
• Facultative intracellular bacteria
• Resemble safety pin in stained
preparation
• Has three kinds of plasmids
• Smallest is Pla
• Causes protective clots to
dissolve via activation of
plasminogen activator
• Middle plasmid codes Yops proteins
and regulators of Yops proteins
• Yops interferes with phagocytosis
• Last is F1
• Becomes anitphagocytic capsule
• Used in plague vaccine
Plague (Black Death)
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Pathogenesis
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Masses of organism obstruct digestive tract of rat fleas
Flea regurgitates infected material into bite wound
Pla is essential to spread from site of entry
Organisms multiply within macrophages
• Produce F1 capsule while in macrophages
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Macrophages die and release organism
• Organism encapsulated and produces Yops proteins and other mechanisms that enhance
survival
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Inflammation in nodes results in characteristic swelling
• Nodes become necrotic and spill organisms
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Septicemic plague
Mortality rate of untreated reaches between 50% and 80%
Plague (Black Death)
• Epidemiology
• Endemic on rodent populations in all continents
except Australia
• Prairie dogs, rock squirrels and their fleas are
main reservoir
• Hundreds of fleas can transmit plague and can
remain infectious for a year
• Can spread person to person by household fleas
• Organism can remain viable for weeks in dried
sputum and flea feces
Plague (Black Death)
• Prevention and Treatment
• Prevention directed by rat control
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Proper garbage disposal
Rat-proof buildings
Guards on mooring ropes
Extermination programs
• Killed vaccine gives short-term partial protection
• Treatment via tetracycline for some exposed
individuals to control epidemics
• Gentimicin, ciprofloxacin and doxycycline
effective on disease if given early
Infectious Mononucleosis
• Symptoms
• Appear after long incubation
• Usually 30 to 60 days post infection
• Symptoms include fever, sore
throat covered with pus, fatigue,
enlarged lymph nodes and spleen
• Most cases fever and sore throat
disappear within 2 weeks, lymph
node enlargement within 3
Infectious Mononucleosis
• Causative agent
• Caused by Epstein-Barr virus
• Double stranded DNA virus
• Belongs to herpesvirus family
• Pathogenesis
• Infection begins in cells of throat and mouth and become latent in
another cell type
• Virus carried to lymph nodes after replication in epithelial cells of
mouth, saliva producing glands and throat
• Infects B lymphocytes
• Infection can be productive or nonproductive
• Productive – kills cells
• Nonproductive – virus is latent
• Virus activates B cells to produce multiple clones
• Clones produce immunoglobulin
Pathogenesis of Epstein-Barr Virus
Infectious Mononucleosis
• Epidemiology
• Distributed worldwide
• Infects individuals in crowded, economically
disadvantaged areas
• Infects at early age without producing symptoms producing
immunity
• More affluent populations missed exposure and lack immunity
• Occurs almost exclusively in adolescents and adults
who lack antibody
• Virus present in saliva for up to 18 months
• Mouth-to-mouth kissing important mode of transmission
• No animal reservoir
Infectious Mononucleosis
• Prevention and Treatment
• Avoiding saliva of another person
• No vaccine
• Acyclovir inhibits productive infection
• Has no activity on latent viruses
Yellow Fever
• Symptoms
• Disease can range from mild to severe
• Most common form may be only fever and
slight headache lasting a day or two
• Severe disease characterized by high fever,
nausea, nose bleeds and bleeding into the skin,
“black vomit” from GI bleeding and jaundice
• Mortality rate of severe disease can reach 50%
• Reason for the variation in symptoms is
unknown
Yellow Fever
• Causative agent
• Enveloped, single stranded RNA arbovirus
• Belongs to flavivirus family
• Virus multiplies in mosquitoes
• Mosquitoes transmit virus to humans
• Pathogenesis
• Introduce via bite of Aedes mosquitoes
• Multiplies and enters blood stream
• Carried to liver
• Jaundice results in liver damage
• Injury to small blood vessels produces petechiae
• Kidney failure is a common consequence of disease
Yellow Fever
• Epidemiology
• Reservoir mainly infected mosquitoes and primates in
tropical regions of Central and South America and
Africa
• Periodically spread to urban areas via mosquito bite
• Prevention and Treatment
• Control achieved by spraying and elimination of
breeding sites
• Control almost impossible in jungle regions
• Attenuated vaccine available for high risk groups
• No proven antiviral treatment
Malaria
• Symptoms
• “flu-like”
• Includes fever, headache and pain in the joints and
muscles
• Generally begin 2 weeks post infection
• Transmission via bite of infected mosquito
• Symptom pattern changes after 2 to 3 weeks
• Fall into three categories
• Cold phase – abruptly feels cold and develops shaking
• Hot phase – follows cold phase
• Temperature rises steeply reaching 104°F
• Wet phase – follows hot phase
• temperature falls and drenching sweat occurs
Malaria
• Causative agent
• Human malaria caused by
four species of genus
Plasmodium
• P. vivax, P. falciparum, P.
malatiae, P. ovale
• Infectious form of parasite
injected via mosquito
• Carried by bloodstream to
liver
• Infects cells of liver
• Thousands of offspring
released to produce
infection in erythrocytes
Malaria
• Pathogenesis
• Characteristic feature
• Recurrent bouts of fever followed by times of wellness
• Caused by erythrocytic cycle of growth and release of offspring
• Each species has different incubation periods, degrees
of severity and preferred host age and range
• Spleen enlarges to cope with large amount of foreign
material and abnormal RBC
• Common cause of splenic rupture
• Parasites cause anemia by destroying red RBC and
converting iron from hemoglobin to no-usable form
• Stimulates immune system
• Overworked immune system fails and immunodeficiency
develops
Malaria
• Epidemiology
• Once common in both temperate and tropical
areas
• Now dominantly disease of warm climate
• Eliminated from continental U.S. in late 1940’s
• Mosquitoes of genus Anopheles are biological
vectors
• Infected mosquitoes and humans constitute
reservoir
• Transmission via mosquitoes, blood transfusion
and sharing of syringes
Malaria
• Prevention and Treatment
• Treatment is complicated
• Due to different stages of mosquito life cycle
• Chloroquine
• Effective against erythrocyte stage
• Will not cure liver infection
• Primaquine and tafenoquine
• Generally effective against exoerythrocyte stage and
certain species gametocytes