Diphtheria Pertussis Tetanus

8/20/2019 Diphtheria Pertussis Tetanus

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DIPHTHERIA,PERTUSSIS &

TETANUS

Dr Sarika Gupta, Asst. Professor


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Diphtheria (Corynebacterium diphtheriae)

Diphtherais Greek wor for !eather

Bull-neck appearance of diphtheriticcervical lymphadenopathy


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INTR"DU#TI"N

An acute to$i% infection caused by Corynebacterium

diphtheriae and rarely toxigenic strains of Corynebacterium

ulcerans

aerobic, nonencapsulated, non–spore-forming, mostly

nonmotile, pleomorphic, gram-positive bacilli

Differentiation of C. diphtheriae from C. ulcerans is based on

urease activity, C. ulcerans is urease-positive

Four C. diphtheriae biotypes - mitis, intermedius, belfanti,gravis; differentiated by colonial morphology, hemolysis, and

fermentation reactions


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INTR"DU#TI"N

Diphtheritic toxin production occurs only after acuisition of a

lysogenic Corynebacteriophage by either C. diphtheriae or C.

ulcerans, !hich encodes the diphtheritic toxin gene and confers

diphtheria-producing potential on these strains

Demonstration of diphtheritic toxin production or potential

for toxin production by an isolate is necessary to confirm

disease

"he former is done in vitro using the agar immunoprecipitin

techniue (E!ek test) or in vivo !ith the toxin neutrali#ationtest in guinea pigs, the latter by polymerase chain reaction

testing for carriage of the toxin gene

Toxin is lethal in human beings in an amount 130μg/kg B


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EPIDEI"'"G

Tras*issio+ airborne respiratory droplets, direct contact

!ith respiratory secretions of symptomatic individuals, or

exudates from infected s$in lesions

!symptomatic respiratory tract carriage is important in

transmission" %here diphtheria is endemic, -/ of healthy

individuals can carry toxigenic organisms

Diphtheria is ee*i% i INDIA.

&$in infection and s$in carriage are silent reservoirs andorganisms can remain viable in dust or on fomites for up to

' months

"ransmission through contaminated mil$ and an infected food

handler has been documented


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EPIDEI"'"G

Children aged (-)yrs are commonly infected

A herd immunity of *+ is reuired to prevent epidemics

Contaminated obects li$e thermometers, cups, spoons, toysand pencils can spread the disease

vercro!ding, poor sanitation and hygiene, illiteracy, urban

migration and close contacts can lead to outbrea$


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PATH"GENESIS


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'o%a! effe%t of iphtheriti% to$i+

/aralysis of the palate and hypopharynx

/neumonia

S0ste*i% effe%ts (To$i a1sorptio )+ $idney tubule necrosis

hypoglycemia

myocarditis and0or demyelination of nerves

0o%aritis+23-24 a0s

De*0e!iatio of er5es+ -6 weeks


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#'INI#A' ANI7ESTATI"NS

1nfluenced by the anatomic site of infection, the immune

status of the host and the production and systemic distribution

of toxin

I%u1atio perio+ (-' days

#!assifi%atio (!o%atio)+

nasal

pharyngeal

tonsillar laryngeal or laryngotracheal

s$in, eye or genitalia


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#asal diphtheria$ 1nfection of the anterior nares- more

common among infants, causes serosanguineous, purulent,

erosive rhinitis !ith membrane formation

&hallo! ulceration of the external nares and upper lip is

characteristic

%nilateral nasal discharge is &uite pathognomic of nasal

diphtheria Accurate diagnosis of nasal diphtheria delayed-paucity of

systemic signs and symptoms


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Tonsillar and pharyngeal diphtheria$

sore throat is the uni'ersal early symptom

nly half of patients have fever and fe!er have dysphagia,

hoarseness, malaise, or headache 2ild pharyngeal inection unilateral or bilateral tonsillar

membrane formation extend to involve the uvula, soft

palate, posterior oropharynx, hypopharynx, or glottic areas

3nderlying soft tissue edema and enlarged lymph nodes4 bull(neck appearance


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)aryngeal diphtheria$ At significant ris$ for suffocation

because of local soft tissue edema and air!ay obstruction by

the diphtheritic membrane

Classic cutaneous diphtheria is an indolent, nonprogressive

infection characteri#ed by a superficial, ecthymic, nonhealing

ulcer !ith a gray-bro!n membrane


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*nfection at +ther ,ites$

ear 5otitis externa6, the eye 5purulent and ulcerative

conunctivitis6, the genital tract 5purulent and ulcerative

vulvovaginitis6 and sporadic cases of pyogenic arthritis

Diagnosis

Clinical features

Culture4 from the nose and throat and any other

mucocutaneous lesion. A portion of membrane should beremoved and submitted for culture along with underlying

exudate

7le$ test4 rapid diagnosis 5('-89 hrs6


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7n#yme immunossay

/C: for A or portion of the toxic gene ypoglycemia, glycosuria, 3?, or abnormal 7C@ for liver,

$idney and heart involvement Differetia! ia8osis+

(. Common cold

8. Congenital syphilis snuffle

. &inusitis

9. Adenoiditis and foreign body in nose

. Strepto%o%%a! phar08itis

'. 1nfectious mononucleosis


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#"P'I#ATI"NS

(. :espiratory tract obstruction by pseudomembranes4

bronchoscopy or intubation and mechanical ventilation

8. "oxic Cardiomyopathy4

-in (+-8) of patients

-responsible for )+-'+ of deaths

-the ris$ for significant complications correlates directly !ith the extent

and severity of exudative local oropharyngeal disease as !ell as delay in

administration of antitoxin

-Ta%h0%aria out of proportio to fe5er

-prolonged /: interval and changes in the &"-" !ave

- Elevation of the serum aspartate aminotransferase concentration

closely parallels the severity of myonecrosis


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. "oxic ?europathy4

Acutely or 8- !$ after4 hypoesthesia and soft palate paralysis

After!ards !ea$ness of the posterior pharyngeal, laryngeal, and facial nerves

4 a nasal uality in the voice, difficulty in s!allo!ing and ris$ for aspiration

Cranial neuropathies 5)th !$64 oculomotor and ciliary paralysis- strabismus, blurred vision, or difficulty !ith accommodation

&ymmetric polyneuropathy 5(+ days to mo64 motor deficits !ith diminished

deep tendon reflexes

2onitoring for paralysis of the diaphragm muscle

-eco'ery from the neuritis is often slo. but usually complete"

Corticosteroids are not recommended"


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TREATENT

1" !ntitoxin$

2ainstay of therapy

?eutrali#es o!0 free to$i, efficacy diminishes !ith elapsed time

Antitoxin is administered as a single empirical dose of 8+,+++-

(8+,+++ 3 based on the degree of toxicity, site and si#e of the

membrane, and duration of illness

" !ntimicrobial therapy

>alt toxin production, treat locali#ed infection and prevent transmission

of the organism to contacts er0thro*0%i 59+-)+ mg0$g0day ' hrly B/ or B16, aueous

%r0sta!!ie pei%i!!i G 5(++,+++-()+,+++ 30$g0day ' hrly 1 or B126,

or pro%aie pei%i!!i 58),+++-)+,+++ 30$g0day (8 hrly 126 for 24 a0s


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7limination of the organism should be documented by

negative results of at least 8 successive cultures of specimens

from the nose and throat 5or s$in6 obtained 89 hr apart after

completion of therapy

rognosis$ depends on the virulence of the organism

5subspecies gravis6, patient age, immuni#ation status, site of

infection and speed of administration of the antitoxin

"he case fatality rate of almost (+ for respiratory tract

diphtheria

At recovery, administration of diphtheria toxoid is indicated to

complete the primary series or booster doses of immuni#ation,

because not all patients develop antibodies to diphtheritic

toxin after infection


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PRE9ENTI"N

!symptomatic Case Contacts$

Antimicrobial prophylaxis -er0thro*0%i 59+-)+ mg0$g0day divided id

/ for 23 a0s6 or a si8!e inection of 1e:athie pei%i!!i G

5'++,+++3 12 for patients E+ $g, (,8++,+++3 12 for patients + $g6

Diphtheria to$oi 5a%%ie-to immuni#ed individuals !ho have notreceived a booster dose !ithin ) yr. Children !ho have not received their

9th dose should be vaccinated. "hose !ho have received fe!er than

doses of diphtheria toxoid or !ho have uncertain immuni#ation status are

immuni#ed !ith an age-appropriate preparation on a primary schedule

!symptomatic Carriers$ &ameG:epeat cultures are performed about 8 !$ after completion of

therapy. if results are positive, an additional (+-day course of oral

erythromycin should be given and follo!-up cultures performed

!CC*#2


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;hoopi8 %ou8h+ whoopi8 sou *ae whe8aspi8 for air after a fit of %ou8hi8

#ou8h of 233 a0s

PERTUSSIS (;H""PING #"UGH)


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INTR"DU#TI"N

A highly contagious acute bacterial infection caused by the

bacilli Bordetella pertussis

Currently !orld!ide prevalence is diminished due to active

immuni#ation

>o!ever it remains a public health problem among older

children and adults

*t continues to be an important respiratory disease afflicting

un'accinated infants and pre'iously 'accinated children and

adults .aning immunity4


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EPIDEI"'"G

Tras*issio+ through the respiratory route in the form of

droplet infection

Adolescents and adults are the reservoir. ?o animal or insectreservoir

A highly communicable disease. &A: H+ among

households contacts

1n the catarrhal stage and 8 !ee$s after the onset of cough


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ETI"'"G

Bordetella pertussis – aerobic gram-negative coccobacilli

/roduces to$is namely pertussis toxin, filamentoushemagglutinin, hemolysin, adenylate cyclase toxin,

dermonecrotic toxin and tracheal cytotoxin- responsible for

clinical features 5toxin mediated disease6 and the immunity


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PATH"GENESIS


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1ncubation period4 *-(+ days

1nfection lasts for ' !ee$s – (+ !ee$s

Sta8e I (%atarrha! sta8e< 2-= weeks)+ insidious onset of

cory#a, snee#ing, lo! grade fever and occasional cough Sta8e II (paro$0s*a! %ou8h sta8e< 2-> weeks)+ due to

difficulty in expelling the thic$ mucous form the

tracheobronchial tree

At the end of paroxysm long inspiratory effort is follo!ed bya !hoop

1n bet!een episodes child loo$ !ell. During episode of cough

the child may become cyanosed, follo!ed by vomiting,

exhaustion and sei#ures


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Cough increase for next 8- !ee$s and decreases over next (+

!ee$s

Absence of !hoop and0or post-tussive vomiting does not ruleout clinical diagnosis of pertussis

paroxysmal cough5 .eeks .ith or .ithout .hoop and/or

post(tussi'e 'omiting is the hallmark feature of pertussis

Sta8e III (%o5a!e%e%e sta8e)+ period of gradual recoveryeven up to ' months


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#"P'I#ATI"NS

(. &econdary pneumonia 5( in )6 and apneic spells 5)+;

neonates and infantE' months of age6

8. ?eurological complications4 sei#ures 5( in (++6 and

encephalopathy 5( in ++6 due to the toxin or hypoxia or

cerebral hemorrhage

. titis media, anorexia and dehydration, rib frcture,

pneumothorax, subdural hematoma, hernia and rectal prolapse

Differential diagnosis$

(. . parapertussis, adenovirus, mycoplasma pneumonia, and

chlamydia trachomatis

8. 7orei8 1o0 aspiratio, endobronchial tuberculosis and a

mass pressing on the air!ay


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DIAGN"SIS

(. &uspected on the basis of history and clinical examination

and is confirmed by culture, genomics or serology

8. 7levated %C count !ith lymphocytosis. "he absolute

lymphocyte count of ?=3,333 is highly suggestive. Culture4 gold standard specially in the catarrhal stage. A

saline nasal s!ab or s!ab from the posterior pharynx is

preferred and the s!ab should be ta$en using dacron or

calcium alginate and has to be plated on to the selectivemedium


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DIAGN"SIS

However culture are not recommended in clinical practice as

the yield is poor because of previous vaccination, antibiotic

use, diluted specimen and faulty collection and

transportation of specimen.

9. /C:4 most sensitive to diagnose; can be done even after

antibiotic exposure. It should always be used in addition with

cultures

). Direct fluorescent antibody testing4 lo! sensitivity and

variable specifity


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TREATENT

(. Avoidance of irritants, smo$e, noise and other cough

promoting factors

8. Antibiotics4 effective only if started early in the course of

illness. Er0thro*0%i 59+-)+ mg0$g0day ' hrly orally for =

weeks or A:ithro*0%i (+ mg0$g for a0s in childrenE'

months and for childrenI' months (+ mg0$g on day (,

follo!ed by )mg0$g from day8-) or #!arithro*0%i ()

mg0$g (8 hrly for 6 a0s

. &upplemental oxygen, hydration, cough mixtures and

bronchodilators 5in individual cases6


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PRE9ENTI"N

All household contacts should be given erythromycin for 8

!ee$s

Children E* years of age not completed the four primary dose

should complete the same at the earliest

Children E* years of age completed primary vaccination but

not received the booster in the last years have to be given a

single booster dose

ACC1?7


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Tetaus

JCKLA%


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INTR"DU#TI"N

"etanus is an acute, fatal, severe e$oto$i mediated nervous

system disorder characteri#ed by muscle spasm

Caused by the toxin producing anaerobe, Clostridium tetani Tetanus is the only 'accine pre'entable disease that is

infectious but not contagious from person to person


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EPIDEI"'"G

C. tetani is a part of the normal flora in human and animal

intestines and is disseminated through excreta

1n spore form they are hard and long lasting in soil and dust "he contamination of !ound, unhygienic and improper

handling of the umbilical cord in ne!borns, lac$ of hygienic

habits and aseptic care during and after delivery are the main

ris$ factors for infection


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PATH"GENESIS


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PREDISP"SING 7A#T"RS

A penetrating inury – inoculation of C. tetani spores

Coinfection !ith other bacteria

Devitali#ed tissue A foreign body

Jocali#ed ischemia

Therefore tetanus de'elop in these clinical settings4

neonates, obstetric patients, postsurgical patients, patients!ith dental infection, diabetic patients !ith infected extremity

ulcers, patients !ho inect illicit and0or contaminated drugs


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1ncubation period4 (-H days

Geera!i:e tetaus+

/resenting feature is trismus

&ymptoms of autonomic overactivity such as irritability,restlessness, s!eating, tachycardia, cardiac arrhythmias, labile

hypotension or hypertension and fever

"onic contractions of s$eletal muscles 5stiff nec$,

opisthotonus, risus sardonicus, board li$e rigid abdomen6 andintermittent intense muscular spasms !ith no impairment of

consciousness

/ainful spasms, triggered by loud noises or other sensory

stimuli such as physical contact or light


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/eriod of apnea and0or upper air!ay obstruction due to

contraction of thoracic muscles and0or glottal or pharyngeal

muscle

Neoata! tetaus+

2anifested by rigidity, spasms, trismus, inability to suc$ and

sei#ures

Diagnosis$ mainly clinical


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TREATENT

est in the 1C3 as child may need early and aggressive

air!ay management

"he goals of treatment include

2.

Ha!ti8 to$i prou%tio %ound debridement

Antimicrobial therapy4 *etroia:o!e or pei%i!!i @ for 6-

23 a0s

=. Neutra!i:atio of u1ou to$i+ >"1@-,+++-',+++ units i.m.

7uine antitoxin (,)++-,+++ units i.m. or i.v.


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TREATENT

. #otro! of *us%!e spas*s

Avoidance of sensory stimuli

&edatives4 dia#epam

4. aa8e*et of autoo*i% 0sfu%tio+ 2agnesium sulfate, beta bloc$ers, morphine sulfate

. Airwa0 *aa8e*et a other supporti5e *easures

ai treat*et as bound tetanus toxin can not be displaced

from the nervous system 7ndotracheal intubation0tracheostomy, nutritional support,

physical therapy as soon as spasms have ceased


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PRE9ENTI"N

1mmuni#ation and proper treatment of !ounds and traumatic

inuries

-+6#+,*,$

"he average mortality of tetanus is 9)-)) ?eonatal tetanus4 '+-*+

2ost important factor influencing outcome is supportive care


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PRE9ENTI"N

!CC*#2$

D/" vaccine4 primary doses starting at ' !ee$s of age

(st booster at ('-(H months of age, 8nd booster at ) years of

age At (+ years of age "dap0"d follo!ed by "d every (+ years

Catch-up vaccination4

elo! * years4 D/" at +,( and ' months

Documents

Diphtheria Pertussis Tetanus