Upper Respiratory Tract Infections - PDF

UPPER RESPIRATORY TRACT INFECTIONS Dr. Khadiga M. Mansur 1  Learning outcome ’ Discuss different microbial pathogens of the upper respiratory tract including pharyngitis, croup, and Epiglottitis with emphasis onH. influenzae ’ Describe the causes, manifestations...

UPPER RESPIRATORY TRACT INFECTIONS Dr. Khadiga M. Mansur 1  Learning outcome ’ Discuss different microbial pathogens of the upper respiratory tract including pharyngitis, croup, and Epiglottitis with emphasis onH. influenzae ’ Describe the causes, manifestations, diagnosis, treatment, and prevention of throat infections with emphasis on Corynebacterium diphtheriae ’ Describe the causes, manifestations, diagnosis, treatment, and the possibilities for preventing pertussis 2  Corynebacterium ’ Corynebacterium is gram-positive bacilli with an irregular shape, tendency to clubbing at one or both, highly pleomorphic with Chinese letter or cuneiform arrangement. ’ Two media are useful. 1. Loeffler’s serum slope tellurite blood agar ’ Fermentations of sugars are usually done in Hiss’s serum peptone water medium ’ C. diphtheriae is H2S positive and reduces nitrate to nitrite ’ Toxin: Toxigenic strains of C. diphtheriae produce a very powerful exotoxin. ’ The toxigenicity of the diphtheria bacillus depends on the presence in it of corynephages (tox+). 3  Corynebacterium ’ The toxigenicity of the diphtheria bacillus depends on the presence in it of corynephages (tox+). ’ Diphtheria toxin is, heat labile protein, and consists of two fragments. ’ Inhibition of protein synthesis is probably responsible for both the necrotic and neurotoxic effects of the toxin ’ Clinical diseases: Diphtheria occurs in two forms ’ (respiratory and cutaneous) ’ Laboratory diagnosis: Depends upon microscopy, culture and virulence tests. Virulence testing may be by in vivo or in vitro methods. 4 ’ Diphtheria manifests as sore throat, localized pain, fever, pharyngitis, and the oozing of a fluid in the throat composed of intracellular fluid, blood clotting factors, leukocytes, bacteria, and the remains of dead pharyngeal and laryngeal cells. ’ The fluid thickens into a thick pseudomembrane. 5  ’ pseudomembrane can adhere so tightly to the tonsils, uvula, roof of the mouth, pharynx, and larynx that it cannot be dislodged without ripping the underlying tissue and causing bleeding. In severe cases, the pseudomembrane can completely block the respiratory passages, resulting in death by suffocation 6  Corynebacterium 7  Corynebacterium ’ In vivo tests are i. Subcutaneous test; ii. Intracutaneous test. ’ In vitro test include i) Precipitation test; ii) Tissue culture test; iii) Enzyme-linked immunosorbent assays (ELISA); iv) Polymerase chain reaction (PCR) ’ Prophylaxis: DPT given at the age of 6 weeks, 10 weeks, 14 weeks and 16–24 months followed by booster dose DT at the age of 5–6 years (school entry) ’ Diphtheroids: Corynebacteria resembling C. diphtheriae occur as normal commensals in the throat, skin and other areas. ’ These may be mistaken for diphtheria bacilli and are known as diphtheroids. ’ The common diphtheroids are C. Pseudodiphtheriticum and C. xerosis 8  Bordetella pertussis ’ The genus Bordetella constitutes a group of minute, gram-negative, non-acid-fast, non-sporing, coccobacilli. ’ Three important species of Bordetella include Bordetella pertussis, B. parapertussis and B. Bronchiseptica B. pertussis are extremely small, ovoid, gram-negative ’ coccobacilli showing pleomorphism; nonmotile and nonsporing 9  Bordetella pertussis ’ Two adhesins are filamentous hemagglutinin and pertussis toxin. ’ Four toxins are: ’ Pertussis toxin, a portion of which interferes with ciliated epithelial cells’ metabolism, resulting in increased mucus production. (Note that pertussis toxin is both an adhesin and a toxin.) ’ Adenylate cyclase toxin, which triggers increased mucus production and inhibits leukocyte movement, phagocytosis, and killing. ’ Dermonecrotic toxin, which causes localized constriction and hemorrhage of blood vessels, resulting in cell death and tissue destruction. ’ Tracheal cytotoxin, which at low concentrations inhibits the movement of cilia on respiratory cells. 10  Bordetella pertussis ’ Bordetella pertussis are strict aerobes and nutritionally fastidious, grow on specialized media such as Bordet– Gengou agar and charcoal agar with 10% blood ’ B. pertussis produces a number of factors that are involved in the pathogenesis of disease, such as pertussis toxin (PT) ’ Diseases: Pertussis and is characterized by three ’ stages: catarrhal, paroxysmal, and convalescent stages. Children younger than 1 year at greatest risk for infection ’ Laboratory diagnosis: Depends on microscopy, ’ culture and polymerase chain reaction (PCR) ’ Treatment with macrolide (i.e. erythromycin, azithromycin) is effective in. Erythromycin has been used for prophylaxis 11  Bordetella pertussis  Vaccination with whole-cell vaccines is effective but associated with side effects. Acellular vaccines are effective and associated with fewer adverse effects‫ز‬ ’ Catarrhal stage begins with signs and symptoms resembling the common cold that last one to two weeks. ’ Thefollowing paroxysmal stage lasts two to four weeks and is characterized by persistent, violent coughing spells that consist of three or four coughs without a breath, followed by a high-pitched, wheezing inhalation or “whoop.” The convalescent stage lasts several weeks as the cough subsides. 12 ’ Incubation period 6–20 days, with an average of 7–10 days.  ’ Susceptibility Unimmunized children. ’ Treatment Supportive care; erythromycin has only little effect. ’ Prevention DTaP vaccine 13  EPIGLOTTITIS ’ Definition Epiglottitis is an inflammation of the epiglottis. ’ Clinical Manifestations ’ Patients present with rapidly worsening sore throat and odynophagia (pain on swallowing) or dysphagia (difficulty in swallowing). Pain may be out of proportion to physical examination findings. Airway obstruction can occur in severe cases. Epiglottitis in young children should betreated as a medical emergency. ’ Pathogens Haemophilus influenzae type B is, by far, the most common cause, although the widespread use of the vaccine against H. influenzae type B has greatly reduced the incidence of epiglottitis. Less common pathogens include other H. influenzae types, S. pneumoniae, S. pyogenes, and S. aureus. 14  Haemophilus influenzae ’ Diseases—Sinusitis, otitis media, and pneumonia are common. ’ Epiglottitis is uncommon, but H. influenzae is the most important cause. Haemophilus influenzae used to be a leading cause of meningitis, but the vaccine has greatly reduced the number of cases. ’ Characteristics—Small gram-negative (coccobacillary) rods. Requires factors X (hemin) and V (NAD) for growth. Of the six capsular polysaccharide types, type b causes 95% of invasive disease. Type b capsule is polyribitol phosphate. ’ Habitat and Transmission—Habitat is the upper respiratory tract. Transmission is via respiratory droplets. ’ Pathogenesis—Polysaccharide capsule is the most important determinant of virulence. Unencapsulated (“untypeable”) strains cause mucosal infections but not invasive infections. IgA protease is produced. 15  ’ Most cases of meningitis occur in children younger than 2 years of age, because maternal antibody has waned and the immune response of the child to capsular polysaccharides can be inadequate. No exotoxins identified. ’ Laboratory Diagnosis—Gram-stained smear plus culture on chocolate agar. Growth requires both factors X and V. Determine serotype by using antiserum in various tests (e.g., latex agglutination). Capsular antigen can be detected in serum or cerebrospinal fluid. Serologic test for antibodies in patient’s serum not useful. ’ Treatment—Ceftriaxone is the treatment of choice for meningitis. Approximately 25% of strains produce β-lactamase. ’ Prevention—Vaccine containing the type b capsular polysaccharide conjugated to diphtheria toxoid or other protein is given between 2 and 18 months of age. Rifampin can prevent meningitis in close contacts 16  Satellitism phenomenon Sheep blood agar contains hemin but not NAD, Several bacterial species including Staphylococcus aureus, produce NAD as a metabolic byproduct,therfore tiny colonies of Haemophilus spp. May be seen growing on blood agar very close to colonies that can 17 produce V factor  H. Influenzae On Chocolate agar 18  Resources ’ Levinson, Warren. Review of medical microbiology and immunology.23 rd ed. The McGraw-Hill Companies, 2008. ’ Bauman, Robert W., Elizabeth Machunis-Masuoka, and Cecily D. Cosby. Microbiology: With diseases by body system. 4 ed. Benjamin Cummings, 2012. th 19