Mind map bacterial respiratory tract infections (group g)

Mind map bacterial respiratory tract infections (group g)

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  otitis externa otitismedia Bronchiolitis Bronchitis AETIOLOGY CLINICAL MANIFESTATIONS PREVENTION AND TREATMENTS PATHOGENESIS BACTERIAL RESPIRATORY TRACT INFECTIONS sinusitis prevention and treatments Beta-lactamase resistant antibiotic such as amoxicillin- clavulanate or a cephalosporin. For chronic sinusitis, irrigation of the affected sinus. Culture from an antral puncture of the maxillary sinus can be performed to identify the causative organism for selecting antimicrobial therapy. Proper care of infectious and/or allergic rhinitis, surgical correction to relieve or avoid obstruction of the sinusal ostia are important. Root abscesses of the upper teeth should receive proper dental care to avoid secondary infection of the maxillary sinuses. clinical manifestation The maxillary and ethmoid sinuses. Frontal sinuses are less often involved and the sphenoid sinuses are rarely affected. Pain, sensation of pressure and tenderness, malaise and low grade fever. Physical examination usually is not remarkable with no more than an oedematous and hyperemic nasal mucosa. In uncomplicated chronic sinusitis, a purulent nasal discharge is the most constant finding. No pain nor tenderness over the sinus areas. Thickening of the sinus mucosa and a fluid level are usually seen in x-ray films or magnetic resonance imaging. aetiology Vasomotor and allergic rhinitis may also be antecedent Predispose: Obstruction of the sinusal ostia due to deviation of the nasal septum, presence of foreign bodies, polyps / tumors Infection of the maxillary sinuses may follow dental extractions or an extension of infection from the roots of the upper teeth. Common: Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis. Other: Staphylococcus aureus, Streptococcus pyogenes, gram-negative organisms and anaerobes. Chronic sinusitis is commonly a mixed infection of aerobic and anaerobic organisms pathogenesis Bacteria impair the ciliary activity of the epithelial lining of the sinuses and increased mucous secretions. obstruction of the paranasal sinusal ostia which impedes drainage. Bacterial multiplication in the sinus cavities, converts mucous to mucopurulent exudates. The pus further irritates the mucosal lining causing more oedema,epithelial destruction and ostial obstruction. Acute sinusitis chronic: mucosal thickening results and the development of mucoceles and polyps may ensue. OTITIS Aetiology Staphylococcus epidermidis, S.aureus, diphtheroids, Propionibacterium acnes S. pneumoniae, H.influenzae and beta-lactamase producing Moraxella catarrhalis. Clinical Manifestations -Acute otitis media occurs most commonly in young children. -Persistent severe earache (crying in the infant) accompanied by fever and vomiting. -Otologic examination reveals a bulging, erythematous tympanic membrane with loss of light reflex and landmarks. -If perforation of the tympanic membrane occurs, serosanguinous or purulent discharge may be present. -obstruction of the eustachian tube, accumulation of a usually sterile effusion in the middle ear results in serous otitis media. -Chronic otitis media: permanent perforation of the tympanic membrane -Furuncles of the external ear, similar to those in skin infection, can cause severe pain and a sense of fullness in the ear canal. -When the furuncle drains, purulent otorrhea may be present. In generalized otitis externa, itching, pain and tenderness of the ear lobe on traction are present. -Loss of hearing may be due to obstruction of the ear canal by swelling and the presence of purulent debris. -Malignant otitis externa tends to occur in elderly diabetic patients. It is characterized by severe persistent earache, foul smelling purulent discharge and the presence of granulation tissue in the auditory canal. -The infection may spread and lead to osteomyelitis of the temporal bone or externally to involve the pinna with osteochondritis. . Prevention And Treatment •Topical therapy is usually sufficient and systemic antimicrobials are seldom needed unless there are signs of spreading cellulitis and the patient appears toxic. • Neomycin sulfate, polymyxin B sulfate and corticosteroids used as eardrops, • Acidification of the ear canal by applying a 2% solution of acetic acid topically • If a furuncle is present in the external canal, the physician should allow it to drain spontaneously. • Amoxicillin-clavulanate is acute oral preparations of trimethoprim/sulfamethoxazole, second and third generation cephalosporins, tetracyclines and macrolides can also be used. • Chronic otitis media and frequent recurrences : chemoprophylaxis with once daily oral amoxicillin or trimethoprim/sulfamethoxazole • polyvalent pneumococcal vaccines has been evaluated for the prevention of otitis media in children. However, children under two years of age do not respond satisfactorily to polysaccharide antigens; further, no significant reduction in the number of middle ear infections was demonstrable. Pathogenesis 1.The narrow and tortuous auditory canal is lined by a protective surface epithelium. 2.High temperature and humidity, trauma, allergy, tissue maceration, removal of cerumen and an alkaline pH environment, favor the development of otitis externa. 3.Prolonged immersion in a swimming pool coupled with frequent ear cleansing increases the risk of otitis externa. 4.Acute otitis media commonly follows an upper respiratory infection extending from the nasopharynx via the eustachian tube to the middle ear. 5.Vigorous nose blowing during a common cold, sudden changes of air pressure, and perforation of the tympanic membrane also favor the development of otitis media Pharyngitis pathogenesis viral pathogens invade the mucosal cells of the nasopharynx and oral cavity, resulting in edema and hyperemia of the mucous membranes and tonsils. in the case of group A beta-hemolytic streptococci,invade the mucosa of the upper respiratory tract. clinical manifestations Red, sore, or “scratchy” throat. An inflammatory exudate or membranes may cover the tonsils and tonsillar pillars. Vesicles or ulcers on the pharyngeal walls. fever and systemic manifestations such as malaise, myalgia, or headach Anterior cervical lymphadenopathy that causes difficulty in swallowing prevention and treatments Symptomatic treatment is recommended for viral pharyngitis. The specific antibacterial agents will depend on the causative organism, penicillin G is the therapy of choice for streptococcal pharyngitis. erythromycin, tetracyclines and the new macrolides for mycoplasma and chlamydial infections complications 2 major non-suppurative autoimmune complications Acute rheumatic fever Short period of arthritis and fever followed in ~ 50% of affected by rheumatic heart disease Þ heart valve damage Þ chronic valvular disease (stenosis and/or incompetence) Þ heart failure and/or subacute bacterial endocarditis Acute poststreptococcal glomerulonephritis aetiology .Bacterial, viral and fungal infections , smoking. Group A beta-hemolytic streptococcus or S. pyogenes Corynebacterium diphtheriae causes acute pharyngitis Outbreaks of Chlamydia pneumoniae causing pharyngitis or pneumonitis occurred in military recruits. Mycoplasma pneumoniae and Mycoplasma hominis associated with acute pharyngitis upper respiratory tract infections lower respiratory tract infections 2 classification Pneumonia lobar 1 or more of 5 major lobes of lung Serious primary disease Streptococcus pneumoniae bronchial Begins in bronchi and spread to surrounding tissue toward the alveoli in patchy manner Pneumococci Secondary infection/ exposure to chemical 1.Fibrin deposit 2.solidify 3.consolidation Infant: aspiration of amniotic fluid. Elderly: common clinical manifestations Cough, chest pain, fever, shortness of breath and sputum production. Patients are tachycardic. Headache, confusion, abdominal pain, nausea, vomiting and diarrhea may be present, depending on the age of the patient and the organisms involved. prevention and treatments decision on therapy based on clinical history underlying diseses age previous therapies past pneumonias causative microorganism severity illness clinical symptoms sputum examination geographic location pneumococcal vaccine aetiology streptococcus pneumoniae often associated with streptococcus pyogens pneumoniae haemophilus influenza & klebsiella pneumoniae mycobacterium tuberculosis most common community acquired agent hemorrhagic pneumonitis . common among patients over 50 years old who have chronic obstructive lung disease or alcoholism. empyema aerobic gram negative bacilli Pseudomonas aeruginosa, Escherichia coli,Enterobacter, Proteus, and Klebsiella species nosocomial pneumonias that rarely caused pneumonia in healthy individuals cause pneumonia pathogenesis Infectious agents gain access to the lower respiratory tract by hematogenous seeding inhalation aerosolized material aspiration upper airway flora Bronchitis and Bronchiolitis Aetiology •occasionally by M.pneumoniae •preceded by URTI •combination of environmental factors, such as smoking, and bacterial infection with pathogens such as H influenzae and S pneumoniae. Pathogenesis •When the bronchial tree is infected, the mucosa becomes hyperemic and edematous and produces copious bronchial secretions. • The damage to the mucosa, loss of mucociliary function, destruction of the respiratory epithelium • Chronic bronchitis have an increase in the number of mucus-producing cells in their airways, as well as inflammation and loss of bronchial epithelium Clinical Manifestations •mucopurulent sputum , • incessant cough and •production of large amounts of sputum, particularly in the morning. •Fever, a deepening cough, increased respiratory rate, and restlessness follow. Retractions of the chest wall, nasal flaring, and grunting are prominent findings. • Wheezing or an actual lack of breath sounds may be noted. • Respiratory failure and death may result. Prevention and Treatments •Infants with bronchiolitis initially have inflammation and sometimes necrosis of the respiratory epithelium, with eventual sloughing. • Bronchial and bronchiolar walls are thickened. • Exudate made up of necrotic material and respiratory secretions and the narrowing of the bronchial lumen lead to airway obstruction. • Areas of air trapping and atelectasis develop and may eventually contribute to respiratory failure. 3. Prophylactic antibiotics 1.corticosteroids 2.bronchodilators epiglottitis and laryngotracheitis epiglottitis •Begins with the acute onset of fever, sore throat, hoarseness, drooling, dysphagia and progresses within a few hours to severe respiratory distress and prostration. • “cherry-red” epiglottis. 1.Haemophilus influenzae type b, (particularly in children age 2 to 5 years, less common in adults) •all children with epiglottitis should be observed carefully and be intubated to maintain an open airway as soon as the first sign of respiratory distress is detected. •antibacterial therapy •for prevention, haemophilus influenzae type b conjugated vaccine is recommended for all pediatric patients 1.A viral URI may precede infection with H. influenzae in episodes of epiglottitis. 2.Once H influenzae type b infection starts, rapidly progressive erythema and swelling of the epiglottis ensue, and bacteremia is usually present. laryngotracheitis 1. Haemophilus influenzae type b, 2. GABS, 3. C diphtheriae. •Cold-like symptoms is typical of laryngotracheitis, with rhinorrhea, fever, sore throat and a mild cough. •Tachypnea,a deep barking cough and inspiratory stridor develop •Airway obstruction • antibacterial therapy for H.influenza • For prevention, Haemophilus influenzae type b conjugated vaccine is recommended for all pediatric patients 1.Inflammation and edema involve the epithelium, mucosa and submucosa of the subglottis which can lead to airway obstruction. Floating Topic