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أستاذ المادة بشار صاحب خلف الشمري
6/7/2011 7:59:51 AM
diphtheria (corynebacterium diphtheriae)
diphtheria is an acute toxic infection caused by corynebacterium diphtheria, which is an aerobic, non– spore-forming, gram-positive bacillus. three biotypes (i.e., mitis, gravis, and intermedius), each capable of causing diphtheria. c. diphtheriae is an exclusive inhabitant of human mucous membranes and skin. spread is primarily by airborne respiratory dropinglets, direct contact with respiratory secretions of symptomatic individuals, or exudate from infected skin lesions. asymptomatic respiratory tract carriers are important in transmission. pathogenesis
toxigenic and nontoxigenic c. diphtheriae organisms cause skin and mucosal infection. the organism usually remains in the superficial layers of skin lesions or respiratory tract mucosa, inducing local inflammatory reaction. the major virulence of the organism lies in its ability to produce the potent polypeptide exotoxin, which inhibits protein synthesis and causes local tissue necrosis. within the first few days of respiratory tract infection, a dense necrotic coagulum of organisms, epithelial cells, fibrin, leukocytes, and erythrocytes forms, advances, and becomes a gray-brown adherent pseudomembrane. removal is difficult and reveals a bleeding edematous submucosa. paralysis of the palate and hypopharynx is an early local effect of the toxin. toxin absorption can lead to necrosis of kidney tubules, thrombocytopenia, cardiomyopathy, and demyelination of nerves. because the latter two complications can occur 2–10 wk after mucocutaneous infection, the pathophysiologic mechanism in some cases is suspected to be immunologically mediated.
clinical manifestations
the manifestations of c. diphtheriae infection are influenced by the anatomic site of infection, the immune status of the host, and the production and systemic distribution of toxin.
respiratory tract diphtheria
after an average incubation period of 2–4 days, local signs and symptoms of inflammation develop. infection of the anterior nares, which is more common among infants, causes serosanguineous, purulent, erosive rhinitis with membrane formation. shallow ulceration of the external nares and upper lip is characteristic. in tonsillar and pharyngeal diphtheria, sore throat is a universal early symptom, but only half of patients have fever, and fewer have dysphagia, hoarseness, malaise, or headache. mild pharyngeal injection is followed by unilateral or bilateral tonsillar membrane formation, which extends variably to affect the uvula, soft palate, posterior oropharynx, hypopharynx, and glottic areas. underlying soft tissue edema and enlarged lymph nodes can cause a bull-neck appearance. the leather-like adherent membrane, extension beyond the faucial area, relative lack of fever, and dysphagia help differentiate diphtheria from exudative pharyngitis due to group a streptococcus and epstein-barr virus. infection of the larynx, trachea, and bronchi can be primary or a secondary extension from the pharyngeal infection. hoarseness, stridor, dyspnea, and croupy cough are clues. differentiation from bacterial epiglottitis, severe viral laryngotracheobronchitis, and staphylococcal or streptococcal tracheitis hinges partially on the relative paucity of other signs and symptoms in patients with diphtheria and primarily on visualization of the adherent pseudomembrane at the time of laryngoscopy and intubation.
patients with laryngeal diphtheria are highly prone to suffocation because of edema of soft tissues and the obstructing dense cast of respiratory epithelium and necrotic coagulum. establishment of an artificial airway and resection of the pseudomembrane are lifesaving, but further obstructive complications are common, and systemic toxic complications are inevitable.
cutaneous diphtheria
classic cutaneous diphtheria is an indolent, nonprogressive infection characterized by a superficial, ecthymic, nonhealing ulcer with a gray-brown membrane.
infection at other sites
c. diphtheriae occasionally causes mucocutaneous infections at other sites, such as the ear (otitis externa), eye (purulent and ulcerative conjunctivitis), and genital tract (purulent and ulcerative vulvovaginitis).
toxic cardiomyopathy
toxic cardiomyopathy occurs in approximately 10–25% of patients with diphtheria and is responsible for 50–60% of deaths. the risk for significant complications correlates directly with the extent and severity of exudative local oropharyngeal disease and delay in administration of antitoxin. the first evidence of cardiac toxicity characteristically occurs in the 2nd–3rd wk of illness. tachycardia out of proportion to fever is common and may be evidence of cardiac toxicity or autonomic nervous system dysfunction. a prolonged pr interval and changes in the st-t wave on an electrocardiographic tracing are relatively frequent findings, and dilated and hypertrophic cardiomyopathy detected by echocardiogram have been described. cardiac dysrhythmias can occur, such as first-, second-, and third-degree heart block atrioventricular dissociation and ventricular tachycardia. clinical congestive heart failure may have an insidious or acute onset. elevation of the serum aspartate aminotransferase concentration closely parallels the severity of myonecrosis. recovery from cardiomyopathy is usually complete, although survivors of more severe dysrhythmias can have permanent conduction defects.
toxic neuropathy
acutely or 2–3 wk after onset of oropharyngeal inflammation, hypersthesia and local paralysis of the soft palate occur commonly. weakness of the posterior pharyngeal, laryngeal, and facial nerves may follow, causing a nasal quality in the voice, difficulty in swallowing, and risk of death due to aspiration. cranial neuropathies characteristically occur in the 5th.week. symmetric polyneuropathy has its onset 10 days–3 mo after oropharyngeal infection and causes principally motor deficits with diminished deep tendon reflexes. proximal muscle weakness of the extremities progressing distally and, more commonly, distal weakness progressing proximally have been described. clinical and cerebrospinal fluid findings in the latter are indistinguishable from those of guillain-barré syndrome. paralysis of the diaphragm can ensue. complete recovery is likely.
diagnosis
specimens for culture should be obtained from the nose and throat and any other mucocutaneous lesion. a portion of membrane should be removed and submitted with underlying exudate.
treatment
specific antitoxin is the mainstay of therapy. antitoxin is administered as a single empirical dose of 20,000–120,000u based on the degree of toxicity, site and size of the membrane, and duration of illness. antimicrobial therapy is indicated to halt toxin production, treat localized infection, and prevent transmission of the organism to contacts. only penicillin or erythromycin is recommended erythromycin is marginally superior to penicillin for eradication of nasopharyngeal carriage. appropriate therapy is erythromycin (40–50mg/kg/24hr divided q 6hr po or iv maximum: 2g/24hr), procaine penicillin (25,000–50,000u/kg/24hr divided q 12h im). therapy is given for 14 days. elimination of the organism should be documented by at least two successive cultures from the nose and throat (or skin) obtained 24hr apart after completion of therapy.
asymptomatic case contacts
all household contacts and those who have had intimate respiratory or habitual physical contact with a patient are closely monitored for illness through the 7-day incubation period. cultures of the nose, throat, and any cutaneous lesions are performed. antimicrobial prophylaxis is given, regardless of immunization status, using erythromycin (40–50mg/kg/24hr divided qid po for 7 days maximum: 2g/24hr) or a single injection of benzathine penicillin g (600,000u im for < 30kg, 1,200,000u im for ?30kg). diphtheria toxoid vaccine, in age-appropriate form, is given to immunized individuals who have not received a booster dose within 5 yr. children who have not received their fourth dose should be vaccinated. those who have received fewer than three doses of diphtheria toxoid or who have uncertain immunization status are immunized with age-appropriate preparation on a primary schedule.
asymptomatic carriers
when an asymptomatic carrier is identified, antimicrobial prophylaxis is given for 7 days and an age-appropriate preparation of diphtheria toxoid is administered immediately if a booster has not been given within 1 yr.
pertussis (bordetella pertussis and b. parapertussis)
bordetella organisms are tiny gram-negative coccobacilli that grow aerobically on starch blood agar or completely synthetic media. bordetella pertussis is the sole cause of epidemic pertussis and the usual cause of sporadic pertussis. b. parapertussis is an occasional cause of pertussis. b. pertussis and b. parapertussis are exclusive pathogens of humans. b. bronchiseptica is a common animal pathogen.
pertussis is extremely contagious, with attack rates as high as 100% in susceptible individuals exposed to aerosol dropinglets at close range. neither natural disease nor vaccination provides complete or lifelong immunity against reinfection or disease.
clinical manifestations
classically, pertussis is a 6-wk disease, divided into catarrhal, paroxysmal, and convalescent stages. the catarrhal stage begins after an incubation period ranging from 3–12 days with nondistinctive symptoms of congestion and rhinorrhea variably accompanied by low-grade fever, sneezing, lacrimation, and conjunctival suffusion. as initial symptoms wane, coughing marks the onset of the paroxysmal stage. the cough is first as a dry, intermittent, irritative hack and evolves into the paroxysms that are the hallmark of pertussis.
infants < 3 mo do not display classical stages. cough (expiratory grunt) may not be prominent. whoop (forceful inspiratory gasp) infrequently occurs in infants < 3 mo of age who are exhausted or lack muscular strength to create sudden negative intrathoracic pressure.
in toddlers with similarly insignificant provocation suddenly expresses a machine-gun burst of uninterrupted coughs, chin and chest held forward, tongue protruding maximally, eyes bulging and watering, face purple, until coughing ceases and a loud whoop follows as inspired air traverses the still partially closed airway.
post-tussive emesis is common in pertussis at all ages. post-tussive exhaustion is universal. the number and severity of paroxysms progress over days to a week (more rapidly in young infants) and remain at that plateau for days to weeks (longer in young infants). at the peak of the paroxysmal stage, patients may have more than one episode hourly. as paroxysmal stage fades into the convalescent stage, the number, severity, and duration of episodes diminish. paradoxically in infants, cough and whoops may become louder and more classic in convalescence.
immunized children have foreshortening of all stages of pertussis. in infants younger than 3 mo, the catarrhal phase is usually a few days or not recognized at all when apnea, cyanosis, choking, or gasping cough herald the onset of disease convalescence includes intermittent paroxysmal coughing throughout the 1st year of life, including “exacerbations” with subsequent respiratory illnesses these are not due to recurrent infection or reactivation of b. pertussis.
findings on physical examination generally are uninformative. signs of lower respiratory tract disease are not expected. conjunctival hemorrhages and petechiae on the upper body are common.
diagnosis
pertussis should be suspected in any individual who has pure or predominant complaint of cough, especially if the following are absent: fever, malaise or myalgia, exanthem or enanthem, sore throat, hoarseness, tachypnea, wheezes, and rales.
leukocytosis (15,000–100,000 cells/mm3) due to absolute lymphocytosis is characteristic in the catarrhal stage. absolute increase in neutrophils suggests a different diagnosis or secondary bacterial infection. mild hyperinsulinemia and hypoglycemia is reported only occasionally. the chest radiograph appearance is mildly abnormal in the majority of hospitalized infants. parenchymal consolidation suggests secondary bacterial infection. pneumothorax, pneumomediastinum, and air in soft tissues can be seen occasionally.
isolation of b. pertussis in culture remains the gold standard for diagnosis.
treatment
infants younger than 3 mo are admitted to hospital almost without exception, at between 3 and 6 mo unless witnessed paroxysms are not severe, and at any age if significant complications occur. prematurely born young infants and children with underlying cardiac, pulmonary, muscular, or neurologic disorders have a high risk for severe disease.
typical paroxysms that are not life threatening have the following features:
a) duration less than 45 sec
b) red but not blue color change
c) tachycardia, bradycardia (not < 60 beats/min in infants), or oxygen desaturation that spontaneously resolves at the end of the paroxysm
d) whooping or strength for self-rescue at the end of the paroxysm
e) self-expectorated mucus plug and
f) post-tussive exhaustion but not unresponsiveness.
hospital discharge is appropriate if over a 48 hr period disease severity is unchanged or diminished, no intervention is required during paroxysms, nutrition is adequate, no complication has occurred, and parents are adequately prepared for care at home.
antimicrobial agents
an antimicrobial agent is always given when pertussis is suspected or confirmed for potential clinical benefit and to limit the spread of infection. erythromycin (40–50mg/kg/24hr divided qid po maximum: 2g/24hr) for 14 days is standard treatment. ampicillin, rifampin, and trimethoprim-sulfamethoxazole are modestly active. patients are placed in respiratory isolation for 5 days after initiation of erythromycin therapy.
care of household and other close contacts
macrolide agent should be given promptly to all household contacts and other close contacts, such as those in daycare, regardless of age, history of immunization, or symptoms. close contacts < 7 yr of age who have received less than four doses of pertussis-containing vaccines should have vaccination initiated or continued to complete the recommended series. children < 7 yr of age who received a third dose > 6 mo before exposure or a fourth dose 3 yr before exposure should receive a booster dose.
complications
the principal complications of pertussis are apnea, secondary infections, expected pathogens include staphylococcus aureus, s. pneumoniae, and bacteria of oropharyngeal flora, (such as otitis media and pneumonia), and physical sequelae of forceful coughing. bronchiectasis has been reported rarely after pertussis. increased intrathoracic and intra-abdominal pressure during coughing can result in conjunctival and scleral hemorrhages, petechiae on the upper body, epistaxis, hemorrhage in the central nervous system (cns) and retina, pneumothorax and subcutaneous emphysema, and umbilical and inguinal hernias. laceration of the lingual frenulum is not uncommon. rectal prolapse is distinctly unusual and should elicit evaluation for underlying condition. especially in infants in developing countries, dehydration and malnutrition following post-tussive vomiting can have a severe impact. tetany has been associated with profound post-tussive alkalosis.
cns abnormalities occur at a relatively high frequency and are almost always a result of hypoxemia or hemorrhage associated with coughing or apnea in young infants. apnea or bradycardia or both may result from apparent laryngospasm or vagal stimulation just before a coughing episode, from obstruction during an episode, or from hypoxemia following an episode. lack of associated respiratory signs in some young infants with apnea raises the possibility of a primary effect of pt on the cns. seizures are usually a result of hypoxemia, but hyponatremia from excessive secretion of antidiuretic hormone during pneumonia can occur.
المادة المعروضة اعلاه هي مدخل الى المحاضرة المرفوعة بواسطة استاذ(ة) المادة . وقد تبدو لك غير متكاملة . حيث يضع استاذ المادة في بعض الاحيان فقط الجزء الاول من المحاضرة من اجل الاطلاع على ما ستقوم بتحميله لاحقا . في نظام التعليم الالكتروني نوفر هذه الخدمة لكي نبقيك على اطلاع حول محتوى الملف الذي ستقوم بتحميله .
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