LECTURE 10 (Haemophilus, Bordetella & Legionella) Flashcards
Describe Haemophilus
- Gram negative
- Non-motile
- Non-spore forming
- Pleomorphic (appearing in various different forms)
- Appear as “clusters” in infected CSF
- When isolated, capsulated
Describe Haemophilus influenza
- Aerobic gram-negative bacteria
- Polysaccharide capsule (SEROTYPES A-F)
- 95% of invasive disease is caused by type b -> Hit capsule is PRP (Polyribose phosphate capsule)
What is Haemophilus influenza?
A gram-negative, non-motile, coccobacillary bacteria that can cause life threatening infections
EPIDEMIOLOGY:
- strictly human pathogen
- can be found in nasopharyngeal flora of healthy people
- spread by respiratory droplets
- AFFECTS CHILDREN: unvaccinated children under 5 -> invasive disease, meningitis under 2 years, epiglottis + pneumonia in 2-5 year age group
PATHOGENESIS:
- antiphagocytic polysaccharide capsule + endotoxin (no exotoxins!) + lipid A in the cell wall
- IgA protease -> degrades secretory IgA which facilitates attachment to respiratory mucosa
- organisms attach to epithelial cells using PILI + OMP -> invasion takes place between cells by disruption of cell-cell adhesion molecules -> in submucosa, capsule allows bacteria to evade phagocytosis + enter bloodstream
MANIFESTATIONS:
- Meningitis
[Hib meningitis follows pattern of other bacterial meningitis -> preceded by symptoms of upper respiratory infection e.g pharyngitis, sinusitis, otitis media]
- Acute epiglottis
[Sudden onset with fever, sore throat, hoarseness, muffled cough within 24hrs + children have air hunger + inflamed, swollen, cheery-red epiglottis that protrudes into the airway -> visualised on lateral X-rays]
- Pneumonia
- Septicemia
- Cellulitis
- Septic Arthritis
LAB DIAGNOSIS:
- grown on chocolate agar enriched with growth factors, factor X (heme compound) and factor V (NAD)
- biochemical tests/capsular swelling (quellung) reaction -> definitive identification
- fluorescent antibody staining + latex agglutination tests -> detects capsular polysaccharide
TREATMENT:
- Meningitis/systemic infections -> CEFTRIAXONE
[antibiotic treatment is important bc mortality + neurologic sequelae is high]
- Upper respiratory tract infections (e.g otitis media + sinusitis) -> AMOXICILLIN-CLAVULANATE or TRIMETHOPRIM-SULFAMETHOXAZOLE
Describe the difference between the causes of Invasive and localised disease in Haemophilus influenzae
INVASIVE DISEASE = caused by encapsulated strains (mostly type b) -> from nasopharyngeal colonisation site, organisms invade locally to produce CELLULITIS/EPIGLOTTIS -> invasion of blood occurs in all His forms + most frequently leads to meningitis
LOCALISED DISEASE = produced when non-encapsulated strains from the nasopharynx are trapped in the middle ear paranasal sinuses or compromised bronchi
What are the infections caused by the Nontypable strains of Haemophilus Influenzae?
- Otitis media
- Sinusitis
- Pneumonia, Bronchitis (in adults)
How is acute epiglottis treated?
- MEDICAL EMERGENCY -> antimicrobial therapy + maintenance of airway (tracheostomy/endotracheal intubation)
- Manipulations (e.g direct examination/throat swab) can trigger a fatal laryngospasm and acute obstruction
What is Haemophilus Ducreyi?
A gram-negative, coccobacilli bacteria that causes Chancroid (a sexually transmitted genital ulcer in developing countries that is a tender papule on the genitalia that develops into a painful ulcer with sharp margins)
EPIDEMIOLOGY:
- found in Africa, Southeast Asia, India and Latin America
- satellite lesions may develop by autoinfection + regional lymphadenitis is common
- incubation period is 2-5 days
- lack of duration around ulcer is called “soft chancre” which distinguishes it from the primary syphilitic chancre which is indurated + painless
PATHOGENESIS:
- PILI and OMP -> mediate attachment to epithelial cells + resistance to complement-mediated killing
- localises with neutrophils + macrophages but remains extracellular
- secrete antiphagocytic proteins + resists peptides part of innate immune response
DIAGNOSIS:
chocolate agar but grows slowly (genital flora with overgrow plates) so antibiotics must be incorporated
TREATMENT:
- Azithromycin, Ceftriaxone with Ciprofloxacin and Erythromycin
- Condoms
Describe Bordetella Pertussis (Whooping cough)
- Gram negative
- Small, ovoid, coco-bacillus
- Non-motile, non-spore forming
- Survival in environment is very short
- Toxin-mediated disease (produce exotoxins and endotoxins)
What is Bordetella Pertussis (Whooping cough)?
A gram-negative, obligate aerobe, coccobacilli that causes “whooping cough”
CHARACTERISTICS:
- catalase +ve, oxidase +ve, indole -ve, sugars -ve
- growth requires a medium with nutritional supplements (nicotinamide), additives (charcoal) to neutralise inhibitory effect of compounds in bacteriologic media and antibiotics to inhibit other respiratory flora
- growth is slow (3-7 days)
PATHOGENESIS:
- attach to cilia of epithelial cells by FILAMENTOUS HEMAGGLUTININ on pili
[attach to ciliated epithelium but do not invade underlying tissue -> decreased cilia activity + subsequent death of ciliated epithelial cells]
- PERTUSSIN TOXIN
[edema of respiratory mucosa + an A-B subunit toxin that binds to respiratory tract epithelial cells + inhibits signal transduction by chemokine receptors -> failure of lymphocytes to enter lymphoid tissue (spleen + lymph nodes) -> increase in number in blood (LYMPHOCYTOSIS)
- ADENYLATE CYCLASE -> disrupts immune cell function
- TRACHEAL CYTOTOXIN -> fragment of bacterial peptidoglycan that damages ciliated tracheal cells
EPIDEMIOLOGY:
- transmitted by airborne droplets
- highly contagious
- strictly human pathogen
- more than 70% of fatal cases occur in children <1 yr
- incubation period 7-10 days
MANIFESTATIONS:
3 overlapping stages
1) CATARRHAL
[MUCOID RHINORRHEA (mucous out of nose) for 1-2 weeks + malaise, fever, sneezing and anorexia + disease is most communicable at this stage]
2) PAROXYSMAL
[peristent cough + paroxysmal cough (difficulty breathing during coughing) for 2-4 weeks + vomiting + apnea + lymphocytosis]
3) CONVALESCENT
[3-4 weeks, frequency + severity of paroxysmal coughing starts to fade]
LAB DIAGNOSIS:
- Specimens (nasopharyngeal secretions/swabs)
- Culture (charcoal blood agar + cephalosporin, 3-7 days incubation)
- Direct Fluorescent Antibody Test
- Polymerase Chain reaction (PCR)
TREATMENT:
- Azithromycin
- Antimicrobial therapy is useful at earlier stages + limiting spread to susceptible individuals
PREVENTION:
- 2 TYPES OF VACCINES (acellular vaccine = purified proteins from the organism, killed vaccine = inactivated B. pertussis)
- vaccine combined with diphtheria and tetanus toxoids in three doses beginning at 2 months of age
IMMUNITY:
- IgG antibodies produced to Pertussis toxin, pili and pertactin during natural infection + immunisation -> not long-lasting
(second attacks tend to be mild)
Describe Legionella
- Gram-negative
- Do not stain well except with special silver stain (Dieterle silver impregnation stain)
- Aerobic organisms
- Require high concentration of cysteine and iron (cannot be grown in regular labs)
What is Legionella?
Gram-negative bacteria that cause pneumonia-type illnesses such as Pontiac fever and Legionnaires’ disease
EPIDEMIOLOGY:
- not spread from person-to-person but airborne transmission
- found in lakes, hot water tanks of buildings, get into tanks + multiply in sediment, associated with air conditioners + water-cooling towers (AQUATIC)
- common candidate is an older man who smokes and consumes lots of alcohol
PATHOGENESIS:
- Patients who are immunocompromised are predisposed to Legionella pneumonia -> cell-mediated immunity is the most important defence mechanism
- Portal of entry is the respiratory tract + primary changes occur in lung
- Major virulence factor is lipopolysaccharide (endotoxin) -> no exotoxins produced!
- Invade alveolar macrophages for replication
CLINICAL FINDINGS:
- sputum is scanty + non purulent
- Hyponatremia (low sodium)
SYMPTOMS:
can vary from mild influenza-like illness to severe pneumonia accompanied by
- mental confusion
- non-bloody diarrhoea
- protenuria
- microscopic hematuria
LAB DIAGNOSIS:
- Sputum gram stains reveal many neutrophils but no bacteria -> organism grows in culture of sputum or blood on charcoal-yeast agar supplemented with iron and cysteine
- Diagnosis depends on increase in antibody titer in convalascent-phase serum by indirect immunofluorescence assay
- Detection of L. pneumophilia antigens in urine
TREATMENT:
- Azithromyocin/Erythromycin (with or without Rifampin) OR Fluoroquinolones (e.g levofloxacin and trovafloxacin) is treatment of choice
- Penicillins and Cephalosporins are less effective since organism frequently produces B-lactamase
Legionellosis is an _______ _________
Atypical pneumonia
Explanation: It must be distinguish from other similar pneumonias such as Mycoplasma pneumonia, viral pneumonia, psittacosis and Q fever
