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8/6/2019 Haemophilus Etc, Yersinia Etc.
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HaemophilusHaemophilus influenzae
Haemophilus ducreyi
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Haemophilus General Overview
Gram-negative bacilli liking blood (as per genus name)
Obligate Parasites of Man and Animals
Major pathogens for which humans are natural hosts Haemophilus influenzae
Acute pyogenic, normally invasive infections
Chronic infections with H. influenzae as 2o pathogen
Haemophilus ducreyi
STD; Soft chancre (chancroid)
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Chancroid painful genitalulcer with accompanying
painful swollen inguinal
lymph nodes which later
rupture releasing pus
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Syphilitic chancre
painless,
bilateraladenopathy
without pus
Genital Herpes
initially as painful
blisters which later
rupture with
associated
systemic
symptoms
Lymphogranuloma Venereum
(LGV) ulcer disappears
when lymphnodes inflame, LN
are painless and suppurative
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Gardnerella vaginalis
Clue cells vaginalepithelial cells that
contain bacilli within
the cytoplasm
Signs and symptoms: burning or
itching of labia, dysuria, fishyodor foul-smelling vaginal
discharge
Metronidazole drug of choice
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Bordetella pertussis
Fastidious hard to grow like H.influenzae
NOT INVASIVE, meaning never goes into
the bloodstream. It does all its damagewhere it lands in the respiratory tract
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Bordetella pertussis
Virulence FactorsFimbriae for attachment like H. influenzae
Endotoxin role similar to H. influenzae
Big difference between the two is that Bordetella
pertussis produces a bunch of different types ofexotoxins
Pertussis toxin
Increases cAMP in lung cells
Increased cAMP = increased secretion
Excessive mucous and fluid build-up
Adenylate Cyclase Toxin
Also increases cAMP
Dermonecrotic Toxin
Tracheal cytotoxin
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Bordetella pertussis
PathogenesisRespiratory droplet exposure
Enter respiratory tract
Attach to ciliated epithelial cells
Endotoxin inhibits cilia clearance
Replication on outside of respiratory cells
Cells eventually die and release toxin
This is an important point to understand when we talk
about approaches to antibacterial therapy. The cellsmust die and release their toxins to cause the
symptoms of the disease
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Bordetella pertussis
Clinical Infection Whooping cough
Epidemiology
Humans only reservoir
60,000,000 cases annually world wide2000-6000 cases annually in US
Occur primarily in nonimmune children
Adults with waning immunity milderdiseaseMisdiagnosed as cold or flu
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Bordetella pertussis
Three stages of Whooping CoughCatarrhal stageFirst stage as bacteria just start to die and release
toxin
Mild cold symptoms, coughing, sneezing
Child is not that sick so parent thinks they have a
common cold and dont isolate from other children
This is the MOST contagious stage since many
bacteria still alive in respiratory tract and all the
coughing and sneezing spread live bacteria easily to
other children
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Bordetella pertussis
Paroxysmal stageMaximum cell death and toxin release
Severe Cough
40 50 cough spells/day
20-30 coughs in a row with no chance to breath
Coughing causes stomach upset and vomiting
Mucous build-up in Lungs
Air blockage can in rare cases lead to death
Secondary pneumonia is biggest threat
Caused by other bacterial pathogens
H. influenzae, S. aureus, and S. pneumoniae
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Bordetella pertussis
Convalescent stage
Coughing spells diminish slowly
decrease in number of spells andseverity
Possible CNS complications in
some children. The pathogenesis
is not clear
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Bordetella pertussis
TreatmentSelf-limiting in majority of children
Supportive treatment
Antibiotics only speed up the process.Erythromycin (Macrolides)
No effect on disease
Reduces number of live bacteria
Reduces the incidence of secondary pneumoniaProphylaxis of contacts important
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Bordetella pertussis
Vaccination (DPT diphtheria, pertussis, tetanus) Has own unique problems different from the H. influenzae
CNS toxicity was major stumbling block
Blamed on whole cell pertussis prep in the DPT vaccine
Many parents avoided vaccine and apathy led to wide spread
outbreaks
New genetic engineered noncellular preparations have helped to
alleviate fear in parents
However, only effective in 80-85% of children
Therefore, we still need to give antibiotics to contacts
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Legionella sp.
Legionnaires Disease
Pontiac Fever
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Genus Legionella
Best-studied species is L. pneumophila accounts for ~ 85% of infections
motile,Gram-negative, aerobic rod
complex nutritional requirements
~ 50 species in genus, > half implicated in
human disease L. micdadei: mild, febrile, flu-like illness called
Pontiac fever
self-limiting, little or no tissue damage
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Legionella pneumophila
Ubiquitous in soil and freshwater
incidence increased dramatically with installation
of centralA/C
in large buildings grows in A/C cooling towers
aerosols from A/C machinery inhaled
contaminated inhalation therapy devices
dust, liquid aerosols from construction sites
whirlpool spas
colonization of hot water tanks if > 40C
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Legionnaires Disease
Susceptibility
healthy are relatively resistant
impairment of respiratory defenses (heavyalcohol use, smoking, old age) increases
susceptibility
hospital patients with underlying immune
defects also susceptible
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Legionnaires Disease
Fever, disorientation, lethargy
Severe pneumonia progressing to multisystemic
disease
Considerable lung damage
X-rays reveal patches of fluid accumulation
Most invading bacteria found insidephagocytes, growing inside phagosomes
Extensive lysis of phagocytes
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Treatment and Prevention
Drug of choice is erythromycin (why?)
Also azithromcyin, levofloxacin
Prevention: disinfection of water systems
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Yersinia pestis
Gram-negative rod
Intracellular pathogen
Zoonotic infection
Epidemiology
World-wide problem
India has had latest scare (100s infected)
Sporadic cases in the U.S., southwestern
mostly
Usually associated with contact with squirrels
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Yersinia pestis
Clinical Syndromes (Bubonic Plague) Flea bite
Bacilli travel to lymph nodes
Infection results in swelling and pain (Bubo seen in
picture below) High fever, chills, headache, nausea
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Yersinia pestis
Clinical Syndromes (Septicemic Plague)Can penetrate and invade bloodstream
All organs infected
Lungs (secondary pneumonic plague)
Danger to close contacts
50-75% mortality when it goes to
bloodstream
Endotoxin shock primary problem Intravascular coagulation
Multi-organ failure
bruising on skinthis is how it got the name
the black death
See the same thing with Neisseria meningitidis
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Yersinia pestis
Clinical Syndromes (Primary PneumonicPlague)
Spread via respiratory droplets
1 bacilli can cause disease in patient
Severe hemorrhaging
Death in hours
100% mortality if untreated, or late treatment
Diagnosis and Treatment Symptoms and patient history key
Must act fast with treatment
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Brucella species
Medically important species namedfor the livestock they commonly come
from
Brucella abortus (cattle)
Brucella suis (pigs)
Brucella melitensis (goats)
General characteristics Intracellular pathogen
Classic Zoonotic pathogen
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Brucella species
Epidemiology
Worldwide prevalence
Causes serious problems in herds (abortions)
Routes ofTransmission to humans are varied
Unpasteurized Milk (not a real problem in U.S.)
Slaughterhouse, veterinarians, livestock handler
Contact with infected tissue, blood, urine
Inhalation
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Brucella species
Clinical syndrome (undulant fever)
Cyclic undulant fever that lasts for several weeks
Enlarged lymph nodes
Fatigue
Can be chronic long lasting
Diagnosis
Tough because clinical symptoms are so nonspecific
History of patient is most important
Where do they work Where have the traveled (drank unpasteurized milk)
Difficult to culture (takes 6 weeks)
Looking for antibodies in serum also used to diagnose,
but tricky
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Brucella species
Treatment
Tetracycline is drug of choice
Bacteriostatic protein synthesis inhibitor
Good intracellular penetrationRelapses are still common though
Prevention
No vaccine for humans, some for animals
Kill infected animals and herds1000s in killed in Yellowstone National Park
Pasteurize milk and wear protective
clothing
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Francisella tularensis
General characteristics are very similar
to Brucella species
Intracellular pathogen
Zoonotic
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Franciscella tularensis
Epidemiology Worldwide prevalence, widespread in
U.S.
Found in >100 species of animals
(RABBITS) Insect vector important too, and is
something we dont see with Brucella
Routes ofTransmission Infected tissue (rabbit fever)
Inhalation
Ingestion
Insect bites
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Franciscella tularensis
Clinical syndromes (depends on route oftransmission) Ulceroglandular
Most common form of disease (80% of cases)
Ulcer at site of inoculation
Commonly seen in hunters that kill rabbits and skin them This would be the form seen from insect bite as well
Oculoglandular Rub the eye and introduce bacteria into eye
Ulcers in conjuctiva of eye
Pneumonic Highest mortality (10% if untreated) Usually primary inhalation, secondary spread from other
forms
Typhoidal Ingested contaminated meat or water
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Franciscella tularensis
Diagnosis
Clinical history of patient and symptoms
Did they hunt? Insect bite? Skin a rabbit?
Rarely cultured, hard to grow and dangerous to lab
personnel
Treatment
Gentamicin (bactericidal)..tetracycline alternative
Relapses common
Prevention Protect against inoculation
Vaccination of lab personnel only
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Pasteurella multocida
Similar general characteristics to Brucella and
Francisella
Veterinary problem
Both domestic and wild animals
Respiratory/GI during stress (shipping fever)
Cholera in poultry
Hemorrhagic septicemia and pneumonia cattle
Human disease Cellulitis from animal bites
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Pasteurella multocida
Human disease Cellulitis from animal bites
within 24 hours is key for differential diagnosis
Pneumonia from inhalation
S
epticemia and death, this can occur in infants thatare licked by infected dogs or cats in the face
Diagnosis and treatment Patient history
Time of bite critical to differentiate from Grampositive pathogens that take longer to showsymptoms
Penicillin very effective, rare for gram-negativebacteria
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