MUMPS, DIPHTERIA, TETANUS AND PERTUSIS Prof. Dr. Ayça VİTRİNEL.

MUMPS, MUMPS, DIPHTERIA, DIPHTERIA,

TETANUS AND TETANUS AND PERTUSISPERTUSIS

Prof. Dr. Ayça VİTRİNEL

MUMPS Mumps virus RNA virus of the genus

paramyxovirus in the family paramixo-viridae 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 micros-copically.

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 antagonis-tic 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 sardo-

nicus + 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 [3000-6000 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 Corynebacte-

rium diphteriae Gr (+) bacilli, aerobic Three biotypes mitis, gravis-least, intermedius-

most 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.

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 pseudo-membrane is formed that varies from gray to black attemps to remove it are followed by bleeding.

DIPHTERIA

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, pha-

rangitis [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 appere-ance

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

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