MUMPS, DIPHTERIA, TETANUS AND PERTUSIS Prof. Dr. Ayça VİTRİNEL MUMPS Mumps virus RNA virus of the genus paramyxovirus in the family paramixoviridae which also includes parainfluenza viruses. Spread from human reservoir by direct contact, airborne droplets fomites contaminated by saliva and possibly urine. Peak age: 5-9 yr (before vaccinatum) MUMPS Virus has been isolated from as long as 6 days up to 9 days after appereance of salivary gland swelling. Isolated from urine from the 1st –14th day after the onset of salivary gland swelling . Transmission doesn’t seen to occur more than 24 hr before the appereance of the swelling or later than 3 days after it has subsided. MUMPS Clinical Manifestations: Incubation period 14-24 days Prodrome : rare Salivary glands: Pain and swelling in one /both parotid glands Swollen tissues push the ear lobe upward and outward MUMPS Angle of the mandible is no longer visible Swelling subsides within 3-7 days Swollen area is tender and painful pain being elicited especially by tasting sour liquids such as lemon juice or vinegar Redness and swelling about the opening of the Stenon duct are common Edema over the manibrium and upper chest wall may occur lymphatic obstruction. MUMPS Swelling of submandibular glands occur frequently and usually accompany the parotid gland. Least commonly the sublingual glands are infected. MUMPS Diagnosis: Clinical symptoms Physical appereance Laboratory : leukopenia (lymphocytosis) elevations of serum amylase Serology: IgM (in the first days) and IgG Culture: saliva, CSF, blood, urine. MUMPS Treatment: no spesific antiviral treatment Supportive Complications: Meningoencephalomyelitis: most frequently complication. Male/female: 3/1 Primary infection of nerves at the same time or before primer parotitis Postinfectious encephalitis with demyelination follows parotitis by an avarage of 10 days MUMPS Orchitis and epididymitis : adolescent and adults. Follows parotitis within 8 days. Oophoritis Pancreatitis Thyroiditis Myocarditis Deafness Ocular complication Arthritis Prevention: mumps vaccine. TETANUS Acute spastic paralytic illness caused by tetanus toxin (tetanospasmin) a neurotoxin C.tetani Gr (+), spore forming, obligate anaerobe. Natural habitat is soil, dust, alimentary tracts of various animals drumstic/tennis racket appereance microscopically. TETANUS 1) Neonatal 2) Nonneonatal travmatic injury, penetrating injury infected by a dirty object use of contaminated suture material Tetanus toxin binds at the neuromusculer junction endocytosed by the motor nerve axonal transport cytoplasm of motor neuron prevents neurotransmitter release TETANUS Blocks the normal inhibition of antagonistic muscles {basis of voluntary coordinated movement} : affected muscles sustain maximal contraction. Clinical manifestations: 1) Localized 2) generalized: more common TETANUS Incubation period: 2-14 days Trismus (masseter muscle spasm: lockjaw) is presenting symptom Headache, restlessness, irritability stiffness, difficulty chewing, disphagia, sardonic smile Opistotonos : arched posture, neck muscle spasm Laringeal and respiratory muscle spasm : airway obstruction TETANUS Patient remains conscious (tetanus toxin doesn’t affect sensory nerves or cortical function) Smallest disturbance by slight sound, touch : trigger a tetanic spasm Dysuria, urinary retention, forced defecation Fever TETANUS Tachycardia, arythmics Labile hypertension Tetanic paralysis more severe in the 1st week stabilizes in the 2nd week Localized: painful spasm of muscles adjacent to the wound site TETANUS Cephalic tetanus: Rare form of localized tetanus involving the bulbar musculature that occurs with wound or foreign bodies in the head, nostrils or face. Association with chronic otitis media. Retracted eyelids + trismus + risus sardonicus + spastic paralysis of tongue and pharyngeal musculature. TETANUS Neonatal tetanus: 3-12 days after birth Difficulty in feeding Paralysis or diminished movement Stiffness to the touch Diagnosis: Clinically CSF: NORMAL TETANUS Differential diagnosis: acute encephalitis Rabies: CSF pleocytosis, hydrophobia Strychnine poisoning Hypocalsemia Retropharengeal, dental abscess: trismus TETANUS Treatment: eradication of C. tetani Neutralization of all accessible tetanus toxin Control of seizure Supportive care Prevention of recurrences TIG (longer half life): Neutralizes the toxin in the circulation before binding [30006000 U IM recommended ] TETANUS TAT: bovine derived 50.000 – 100.000 U ½ IM + ½ IV risk of serum sickness. IVIG: Contains 4-90 U/ml TIG optimal dosage is not known Antibiotics: Pen G : 100.000 U/kg/ 24 hr : 4-6 hr intervals 10-14 days Metronidazole: 500 mg of 8 hr equally effective Erythromycin and tetracycline are alternative for penicillin allergic patients. TETANUS Muscle relexants: diazepam: relexation and seizure control [0,1-0,2 mg/kg every 3-6 hr IV: 2-6 weeks] { 2yr ; 8mg/kg/day } Baclofen : only in intensive care unit Neromuscular blocking agents M.V. Phenobarbital and morphine may also be used as an adjunctive therapy TETANUS Prognosis: recovery in tetanus occurs through regeneration of synapses, within the spinal cord and restoration of muscle relexation . Episode of tetanus doesn’t result in the production of toxin neutralizing Abs : active immunization with tetanus toxoid at discharge TETANUS Favorable prognosis: long incubation period, absence of fever, localized disease Prevention: active immunization, maternal immunization with at least 2 doses of tetanus toxoid, tetanus prophylaxis in wound management Clean minor wound Other wounds Prior tetanus doses Td TIG Td TIG Uncertain or 3 Yes No Yes Yes Three or more No No No No Yes if 10 yr since last dose Yes if 5 yr since last dose DIPHTERIA Acute toxicoinfection caused by Corynebacterium diphteriae Gr (+) bacilli, aerobic Three biotypes mitis, gravis-least, intermediusmost common Spread by airborne respiratory droplets , direct contact with respiratory droplets, direct contact with respiratory secretions of symp individuals. Exudate from infected skin lesions Asymtomatic respiratory tract carriers are important in transmission. DIPHTERIA Entry of C. Diphtheriae in nose/mouth localized on the mucosal surface of URT toxin is adsorbed to cell membrane tissue necrosis patchy exudate initially be removed As the toxin production increases the area of infection widens and deepens and a fibrinous exudate develops tough adherent pseudomembrane is formed that varies from gray to black attemps to remove it are followed by bleeding. DIPHTERIA Edema of the soft tissues bull neck appereance Clinical manifestations: depend on the site of infection Incubation period: 1-6 days Nasal diphteria: mild rhinorrhea nasal discharge serosaguineous mucopurulent excoriates the nares, upper lip DIPHTERIA White membrane on the nasal septum Most often in infants Slow absorbtion of toxin lack of systemic symptoms Tonsillar and/or pharyngeal diphteria: most common site of disease Anorexia, malaise, low grade fever, pharangitis [1-2 days] thin-gray membrane DIPHTERIA adherent membrane may spread to cover the tonsils and pharyngeal wall may progress [bleeding] in to the larynx and trachea Cervical lymphadenitis : bull neck appereance Respiratory and circulatory collaps may occur Palatal paralysis may occur Stuppor, coma, death : wihin 7-10 days DIPHTERIA Laryngeal diphteria: represents a downward extension of the membrane for the pharynx Occasionally only laryngeal involvement is present Noisy breathing Progresive stridor, hoarseness Suprasternal, subcostal, supraclavicular retractions DIPHTERIA Cutaneous diphteria: an ulcer with a sharpy defined border ,important source of person to person transmission Conjunctival lesions: red, edematous, membranaeous , corneal erosion Aural diphteria: otitis externa with a persistenly purulent and frequently faul smelling discharge DIPHTERIA Diagnosis: isolation of C. diphteria ( Loeffler, tellurite and blood agar) WBC N/ Anemia; result of rapid hemolysis Toxigenicity by inoculating 2 guinea pigs ID suspension of microorganism ( antitoxin/no antitoxin) 24 hr inflamatory lesion , 72 hr necrotic lesion DIPHTERIA Complications: Myocarditis: 2nd week (1-6 wk) ST-T changes 1st degree heart block, hearth failure, myocardial enzymes Neurologic complications: Bilateral, usually resolve competely. Paralysis of the soft palate and pharengeal muscles (1-3 wk ). Ocular muscle and ciliar paralysis (5th wk). Paralysis of diaphragm (5-7 wk). Paralysis of the limbs with loss of deep tendon reflexes (2-7 wk) Elevation of CSF protein, pleocytosis Hypotension, cardiac failure, gastritis, hepatitis, nephritis DIPHTERIA Prevention: Immunization Contacts: Isolation of patient; three consecutive (-) cultures. Cultures schould be taken from close contacts, observed for 7 days if C. diphteria is recovered treatment schould be instituted Asymptomatic immune close contacts: receive a booster of DT, Td, if they haven’t received booster within 5 yr. DIPHTERIA Asymptomatic close contact is not immunized or the immunization status is unknown. He/she should be closely observed and started erythromicin (7 days) or benzathine pen G : culture should be obtained before and after treatment ,active immunization should be given. DIPHTERIA Treatment : Antitoxin must be administired as early as posible by IV route and in a dose sufficient to neutralize all free toxins Desensitization must be done 20.000-40.000 U for pharyngeal/laryngeal 40.000-60.000 U nasopharyngeal 80.000-100.000 U extensive disease DIPHTERIA Penicillin (procain 300.000/600.000 U IM) erythromicin (40 mg/kg/day) 14 days End point of therapy : three consecutive negative culture Bed rest 2-3 wk Hydration Laryngeal diphteria; tracheostomy PERTUSIS = WHOOPING COUGH Acute respiratory infection Bordetella pertusis (B. Parapertusis, B. Bronchiseptica) Gr (-) cocobacils Recovered best in Bordet Gengou media (glyserin, patato, blood agar) Humans are the only known host Spread occurs by direct contact, by respiratory droplets PERTUSIS Transplacental passage of maternal Ab does not protect the NB Severe neonatal pertusis can be acquired from a mildly symptomatic mother. Pathology: peribronchial lymphoid hyperplasia necrotizing process Bronchopneumonia develops with necrosis and desquamation of superficial epithelium of small bronchi. PERTUSSIS Bronchiolar obstruction and atelectasis accumulation of mucus secretions Bronchiectasis may develop Microscobic or gross cerebral hemorrhages may be seen, cortical atrophy has been observed Fatty infiltration of the liver B. Pertussis produces many biologically active factors that are responsible for disease PERTUSIS Pertussis toxin, filamentous hemaglutinin etc Clinical manifestations: inc period : 6-20 days 1) catarhal stage: 1-2 wk rhinorhea, conjuctival injection, lacrimation, mild cough, low grade fever 2) paroxysmal stage: 2-4 wk Repetitive series of 5-10 forceful cough during a single expiration sudden massive inspiratory effort. PERTUSIS Prominent during attack: Facial redness/cyanosis Bulging eyes Protrusion of tongue Lacrimation, salivation Distention of neck veins PERTUSIS Attacks may be trigerred : yawning, sneezing, eating, drinking Petechial/ conjuctival hemorrhages may be noted on the head and neck Diagnosis: cough more than 2 wk duration with posttussive emesis is an important diagnostic clue. PERTUSIS Leukocytosis (20.000-50.000 /mm³) Absolute lymphocytosis Chest roentgen: perihilar infiltrates, atelectasis, emphysema Spesific diagnosis: recovery of the organism nasopharingeal swabs ELISA (IgM, IgG, IgA) PCR PERTUSIS Complications: 1) respiratory: pneumonia, atelectasis, emphysema, pneumothorax, bronchiectasis, otitis media, epistaxis 2) pressure: intracranial hemmorhagea, subconjuctival hemmorhagea, epistaxis, rupture of diaphragma, umbical hernia, inguinal hernia, rectal prolapsus 3) other: convulsions, dehydration, nutritional dis PERTUSIS Prevention: vaccination Erythromycin effective in preventing pertusis. Close contacts of less than 7 yr of age who have been immunized previously booster dose, erythromicin 14 days 7yr , immunized erthromycin 14 days Treatment: erythromycin 50 mg/kg/day (d4) 14 day