Mycoplasma, Bordetella pertussis, and Corynebacterium

does mycoplasma pneumoniae gram stain well?

no, there is no peptidoglycan and it contains sterols in the cell membrane

what is the growing time of mycoplasma pneumoniae?

slow, 1-6hour generation time, and it requires special media containing sterols and lipids to grow

why is it important that mycoplasma pneumoniae does not have a cell wall or peptidoglycan?

antibiotics that target cell wall synthesis are ineffective against it

what is the oxygen preference of mycoplasma pneumoniae?

strict aerobe

what does mycoplasma pneumoniae infect and can people be asymptomatic?

only infects humans, estimated 2 million cases per year, most common age group is 5-15 but everyone is susceptible, outbreaks occur in crowded environments

yes, asymptomatic colonization in the upper respiratory tract is common

how is mycoplasma pneumoniae transmitted?

respiratory droplets to close contacts

how does mycoplasma pneumoniae attach to respiratory tract?

adherence is mediated by a specialized complex of adhesion proteins, organism attaches to a specific sialylated glycoprotein on the surface of both respiratory epithelial cells and erythrocytes, specific attachment at the base of cilia on epithelial cells, attachment and colonization causes ciliastasis and eventually destruction of cilia and ciliated cells

what damage can mycoplasma pneumoniae cause?

characteristic persistent cough, induces inflammatory response which contributes to pathogenesis and clearance, neutralizing antibodies are produced during infection, tracheobronchitis

what is special about the characteristic persistent cough associated with mycoplasma pneumoniae?

loss of ciliated epithelial cells interferes with normal mucociliary clearance of the upper airway, microbes and other particulates can contaminate and irritate lower respiratory tract

what is special about the neutralizing antibodies and autoantibodies that are produced during a mycoplasma pneumoniae infection?

autoantibodies are produced against bacterial glycolipid antigens that cross react with red blood cells resulting in the formation of cold agglutinins

can the 1st mycoplasma pneumoniae infection give you immunity?

no lasting immunity so re-infections can occur

tracheobronchitis

symptoms include low-grade fever, malaise, headache, non-productive cough; pharyngitis may also be present, symptoms gradually worsen over next few days and can persist for 2+ weeks, walking pneumonia

patchy bronchopneumonia

walking pneumonia, potential result of mycoplasma pneumoniae infection

what are the virulence factors of mycoplasma pneumoniae?

adhesins, glycolipids, toxic metabolites, community acquired respiratory distress syndrome toxin, capsular polysaccharides

what is the treatment for mycoplasma pneumoniae?

usually empiric (broad spectrum antimicrobials), no vaccine available

pertussis or whooping cough

disease caused by bordetella pertussis, highly contagious respiratory tract infection, initial symptoms resemble the common cold but with time very serious disease can develop particularly in infants, advanced stages of disease are typified by a severe cough with a high pitched intake of breath that sounds like a whoop

what is the gram status and shape of bordetella pertussis?

gram negative very small coccobacilli

what is the oxygen preference of bordetella pertussis?

strictly aerobic

is bordetella pertussis easy to grow?

no, fastidious and slow-growing, requires special growth media

where can bordetella pertussis be found?

highly contagious disease found worldwide, humans are only reservoir, colonizes the nasopharynx, can be carried asymptomatically

t/f infants are often the source of infection of bordetella pertussis for adults and adolescents

false- opposite

what is the transmission mode of bordetella pertussis?

aerosolized respiratory droplets

who is at the greatest risk of severe disease and death from bordetella pertussis?

children younger than 1 year old

why do bordetella pertussis infections prevalence increase in older children and adults?

waning immunity, emergence of vaccine escape strains, unvaccinated individuals

t/f bordetella pertussis causes most damage from toxin

true- it is primarily a toxin mediated disease

what are the 3 stages of pertussis disease?

catarrhal stage is first, paroxysmal stage is second, convalescent stage is third

catarrhal stage of pertussis disease

1-2 weeks post exposure, resembles the common cold with runny nose, nasal congestion, dry cough, red and watery eyes, sneezing, loss of appetite, mild fever

bacteria present in highest number, highest risk of transmission during this period

paroxysmal stage of pertussis disease

2-4 weeks post exposure, ciliated epithelial cells extruded from respiratory tract and mucus clearance impaired causing airway restriction, repetitive cough with whooping sound, vomiting and leukocytosis

40-50 paroxysms daily at height of illness

in severe cases cyanosis and vomiting, secondary pneumonia, subconjunctival hemorrhages and subdural hematomas can occur

convalescent stage of pertussis disease

3-4 weeks or longer post exposure, paroxysms diminish, secondary complications like pneumonia and seizures can occur

what are the virulence factors of bordetella pertussis?

pertactin and filamentous HA, fimbriae, pertussis toxin, tracheal cytotoxin, and LPS

pertactin and filamentous HA

virulence factor of bordetella pertussis, mediate attachment to ciliated epithelial cells, bind complement receptor 3 on macrophages initiating phagocytosis without an oxidative burst, both are included in acellular vaccines

fimbriae

virulence factor of bordetella pertussis, stimulates humoral immunity, included in acellular vaccines

pertussis toxin

A-B toxin, inhibits phagocytic killing and monocyte migration, PT toxoid included in acellular vaccines

A- activates cell-membrane bound G regulatory proteins

B- binds ciliated respiratory cells and phagocytic cells

tracheal cytotoxin

virulence factor of bordetella pertussis, peptidoglycan monomer with special affinity for ciliated epithelial cells, causes ciliostasis at low concentrations and cell death at high concentrations disrupting normal clearance mechanisms leading to cough, stimulates release of IL-1 causing fever

LPS

virulence factor of bordetella pertussis, activates alternate complement pathway and stimulates cytokine release

how is bordetella pertussis treated?

treatment depends on age and severity of signs as symptoms, can be treated with antibacterial agents to shorten duration of illness and reduce transmission to others and treat severe disease, suportive care with or without antibacterial agents to ameliorate symptoms

when did acellular pertussis vaccines replace whole cell vaccines?

1996

what does the acellular pertussis vaccine contain?

purified inactivated components of bordetella pertussis-pertussis toxin, filamentous HA, and either pertactin and/or fimbriae

what is the pediatric formulation of the pertussis vaccine and how is it administered?

DTaP, 5 shots in the arm at 2, 4, 6, 15-18 months, and then a booster at 4-6 years old

what is the adolescent and adult formulation of the pertussis vaccine and how is it given?

Tdap, immunity wanes at 11 years so booster at 11-18 years old or when indicated, recommended that adults get a booster every 10 years to protect themselves and infants

what is different between DTAP and Tdap

Tdap has reduced amounts of diptheria toxoid compared to DTaP (lower case letters indicated reduced doses)

corynebacterium species

ubiquitous in plants and animals, normally colonize the skin, upper respiratory tract, GI tract, and urogenital tract in humans

t/f most species of corynebacterium diphtheriae cause disease in healthy people

false- most species do not cause disease in healthy, immunocompetent humans, except for certain strains of corynebacterium diphtheriae which can cause diphtheria in non-immune people

what is the gram status and shape of corynebacterium diphtheriae?

gram positive, pleomorphic rods that are club shaped and arranged in clumps and short chains

what is the oxygen preference of corynebacterium diphtheriae?

aerobic

corynebacterium diphtheriae is catalase _____

positive

where is corynebacterium diphtheriae found?

humans are the only known reservoir, asymptomatic carriage in URT, GI tract, UGT or on skin, occurs worldwide but uncommon in places with effective vaccination programs

how is corynebacterium diphtheriae transmitted?

person to person by contact with respiratory secretions or cutaneous lesions

when are people at risk for contracting corynebacterium diphtheriae?

when they are unvaccinated or people with waning immunity at risk when traveling to countries where disease is endemic

what damage can be caused by corynebacterium diphtheriae?

respiratory diphtheria and cutaneous diphtheria

respiratory diphtheria

bacteria attach and multiply locally on epithelial cells in pharynx, release of exotoxin results in local tissue damage

after 2-4 day incubation period, patient experiences sudden onset of pharyngitis with exudate, malaise, and low grade fever

pharyngeal exudate develops into a thick, adherent, gray pseudomembrane

what is dangerous about the pseudomembrane from respiratory diphtheria?

it can extend over the tonsils, uvula, and palate, and into the nasopharynx or larynx

cutaneous diphtheria

acquired through contact with skin from infected people; organism gains access to subcutaneous tissue via breaks in skin, presents as papule that develops into a chronic, non-healing ulcer that may be covered with grayish membrane

what are the virulence factors of corynebacterium diphtheriae?

diphtheria toxin which is an A-B toxin, only strains lysogenized by the bacteriophage carrying the tox gene encoding the exotoxin can produce the toxin, expression of the tox gene is rgulated by the presence of iron; toxin is only produced when iron concentrations are low

A: active toxin which inhibits protein synthesis by inactivating EF-2 which results in cell death

B: subunit binds to specific receptors on target cells and facilitates entry

how can we treat corynebacterium diphtheriae?

usually treat empirically based on clinical presentation because lab tests take too long

diphtheria antitoxin can be given if early, will neutralize toxin before it binds and enters host cells, antibacterial therapy to kill bacteria but this has no effect on toxin already released

supportive care including mainting an open airway

The formation of a gray pseudomembrane which can become dislodged and cause a life-threatening airway obstruction is characteristic of infection with:

A. Neisseria gonorrhea

B. Staphylococcus aureus

C. Streptococcus pneumoniae

D. Corynebacterium diphtheriae

E. Treponema pallidum

D. Corynebacterium diphtheriae

A 23-year-old college student during a regular dental cleaning visit informs about low-grade fever, malaise, and a non-productive cough. Patient complains that these symptoms will not go away and the cough keeps them awake at night. You suspect that the patient has an pneumonia, often called “walking pneumonia”. The organism MOST likely causing this illness is characterized by:

A. the absence of sterols.

B. a Gram-positive cell wall structure.

C. acid-fast cell wall structure.

D. a Gram-negative cell wall structure.

E. the absence of a cell wall.

E. the absence of a cell wall.