Yersinia and Bordetella

Gram-negative coccobacilli

Yersinia and Bordetella

Round/Rod

General Overview – Genus Yersinia

coccobacilli/bacilli

Non-motile, psychrophilic, facultative intracellular anaerobe

Yersinia pestis – Epidemiology and History

Highly virulent pathogen

Lives in small rodents throughout the world

Causes plague – a life threatening bacterial infection

Known as Black Death

High mortality

Y. pestis – Reservoir and Life Cycle

Zoonotic infection

Natural reservoir and biologic vector 

transferred to mammal hosts by flea bite

Y. pestis – Reservoir natural reservoir 

Rodents 

multiples in blood stream, typically subclinical infection

Y. pestis – Reservoir biologic vector

Fleas

Oriental rat flea most efficient vector

Y. pestis – Transmission

Humans are incidental hosts

bite of infected fleas (primary route)

Direct contact

Inhalation of infectious respiratory drops 

3 forms of human disease Y. pestis

Bubonic plague

Septicemic plague

Pneumonic plague

Y. pestis – Clinical Disease

initially “flu-like” symptoms develop after an incubation period of 3-7 days

Bubonic plague

most common form of plague

Septicemic plague

occurs when infection spreads through the bloodstream

Pneumonic plague

most virulent and least common form of plague

high-fatality

spread person to person

Y. pestis – Virulence Factors & Pathogenesis

Molecular pathogenesis complex due to insect (ambient) and mammalian (35-37°C) environments

>20 known virulence factors

Regulatory systems respond to environmental triggers to turn production of necessary virulence factors on or off

4. Examples of factors induced at shift to 37°C:

F1 protein capsule

Adhesins

Type III secretion systems

Yops (Yersinia outer proteins)

Yops (Yersinia outer proteins)

cytotoxic & down-regulate anti-bacterial immune responses

Adhesins

Allow attachment to human cells

Type III secretion systems

Injection of proteins into host cells; cause cellular death

F1 protein capsule

antiphagocytic

Y. pestis – Diagnosis

Laboratory and molecular testing of clinical specimens (fluid from bubos, lungs, or blood)

Y. pestis – Treatment

Rapid diagnosis and initiation treatment with an efficacious antibiotic within 24 hours of symptom onset is critical – plague is a potentially fatal disease

Y. pestis – Prevention

Entrenched in rodent populations globally – unfeasible to eliminate reservoir

Improved sanitation, hygiene, and modern disease control methods have diminished cases

Prophylactic antibiotics prevent infection if you're at risk/been exposed to plague

If you live in / travel to regions where plague is endemic or an outbreak is occurring

Rodent-proof living areas

Keep pets free of fleas

Use insect repellent and protective clothing outdoors

Today Y. pestis is classified as a Category A

(tier 1) biologic agent for potential bioterrorism

Bordetella pertussis

Most important of the 7 species in Bordetella genus

Slow-growing, aerobic, motile, encapsulated, fastidious coccobacillus

Causes pertussis

Strict obligate human respiratory pathogen

pertussis

highly contagious respiratory disease (aka whooping cough)

Hallmark of Bordetella pertussis

severe, spasmodic coughing episodes

Bordetella pertussis – Epidemiology

Major health problem worldwide with ~50 million cases and 300 000 deaths* annually

Highly contagious, infecting more than 90% of exposed susceptible persons

most deaths are among infants

Bordetella pertussis – Virulence Factors & Pathogenesis

Bacteria bind ciliated respiratory epithelium of the upper airway (throat) and lungs

Attachment is mediated by adhesins

Exotoxins are produced

Ciliated cells are destroyed

Body resorts to severe coughing

Attachment is mediated by adhesins

pili, filamentous hemagglutinin (FHA), and pertactin

Exotoxins are produced

damage cells, impair cilia, trigger inflammation, increase mucus, immune evasion

Pertussis toxin (PT)

Tracheal cytotoxin (TCT)

Adenylate cyclase toxin (AC)

Ciliated cells are destroyed

leaving a denuded mucosa without protective and functioning cilia

Body resorts to severe coughing

in attempt to clear damage, excess mucous, and debris

Bordetella pertussis – Clinical Disease

Incubation period typically 7 – 10 days prior to symptom onset

Pertussis follows a prolonged course consisting of 3 overlapping stages

Pertussis 3 stages

Catarrhal

Paroxysmal

Convalescent

Catarrhal

Non-specific cold-like symptoms develop ~1 week after infection

Paroxysmal

Peak coughing; worsen symptoms due to progressively thickened mucus and damaged respiratory epithelium; inspiratory “whoop’

Convalescent

pertussis symptoms gradually fade; secondary pneumonia possible

Bordetella pertussis – Diagnosis

Pertussis symptoms usually diagnostic'

Isolation of B. pertussis from clinical specimen (Catarrhal stage)

Positive NAAT (polymerase chain reaction (PCR)) for B. pertussis

Contact with a laboratory-confirmed case of pertussis

Bordetella pertussis – treatment

Early antibiotic treatment critical (decreased complications, decreased spread)

Supportive care (humidifier, hydration, etc.)

Hospitalization may be required (esp. for infants/young children, compromised, elderly)

Bordetella pertussis – Prevention Vaccination

Immunization most effective method

High efficacy when 1st introduced in DTP vaccine in 1940s
Replaced in mid 1990s with acellular versions (DTaP, Tdap) – parental pressure

(less effective but less side effects)(boosters needed)

Bordetella pertussis – Prevention: Hygiene

As with all respiratory diseases, pertussis is spread by coughing and sneezing (which may be the only symptoms in adults), therefore