haemophilus etc, yersinia etc

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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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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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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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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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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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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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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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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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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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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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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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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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

haemophilus etc, yersinia etc

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