Presented at : To :

Mei 7th, 2018 Masdar Muid, MD. Paed (C)

CASE REPORT I
A 4 YEARS OLD BOY WITH SEVERE DIPHTHERIA
AND ITS COMPLICATIONS

By :
Khodimatur Rofiah

Tutor :
Irene Ratridewi, MD. Paed (C)

THE DEPARTEMENT OF CHILD HEALTH FACULTY

BRAWIJAYA UNIVERSITY MEDICAL FACULTY
Dr. SAIFUL ANWAR GENERAL HOSPITAL
MALANG
2018

0
INTRODUCTION

Diphtheria is an infectious disease, manifests as either upper respiratory tract or

cutaneus infection and is caused by the aerobic gram-positive bacteria,

Corynebacterium diphtheria. People who are most susceptive to infection are those

who are not completely immunized or have low antitoxin antibody levels and have been

exposed to a carrier or diseased individual. C. diphtheriae is aerobic, nonencapsulated,

nonsporeforming, nonmotile, pleomorphic gram-positive bacilli. Pathogen strains can

result in severe localized upper respiratory infection, localized cutaneus infections, and

rarely systemic infection.1,2,

Once a major cause of childhood death, diphtheria was among the first

infectious diseases to be controlled employing modern principles of microbiology,

immunology, and public health. Increased immunization rates, rare circulation of

toxigenic strains, and improved living conditions have controlled diphtheria in

developed countries. While diphtheria is preventable by vaccination, the disease

persists because of regional variations in compliance with vaccination and inadequate

booster regimens. According to the World Health Organization (WHO), 4,500-5,500

cases were reported annually worldwide between 2011 and 2013, with the majority

occurring in India and Indonesia.3,4,5

The disease can result in an acute upper respiratory tract infection

characterised by sore throat, fever (often <38 °C), and an adherent membrane on the

tonsils, pharynx, and/or nasal cavity. The severity of diphtheria is related to the degree

of obstruction of the upper respiratory tract, caused by an acute bacterial toxic

infection, and dissemination of the toxin which can cause myocarditis, polyneuritis, and

other systemic toxic effects. Overall, the case fatality rate may be as high as 20–30% in

toxic forms. The causative bacteria are spread by direct physical contact or breathing

aerosolised secretions.1,4

1
 The purpose of this case report is to discuss patient had complete immunization

but can suffer from severe diphtheria and complication of diphtheria.

CASE REPORT

RZ, 4-year-old boy was admitted to the emergency room at Saiful Anwar

general hospital due to larynx diphtheria referred from Medika Pandaan hospital.

Through anamnesis from his mother, the patient complained dysphagia three days

before admitted (on March 6th, 2018), he also suffered from moderat fever and sore

throat since three days before admitted. The neck looked swollen three days before

admitted. He was confinent breath by mouth since two days before admitted (on March

7th, 2018), stridor, but no dypsnea.

At the first day he got dysphagia, fever, and sore throat. He came to midwife

and got 2 medicines (pulv) but the fever still comes. After 2 days of fever, he came to

Public Health Centers but there was no doctor, so he came to Pediatrician in Pasuruan.

Patient was diagnosed tosilitis and got pulv and mouth drop. And the next day he came

to Purwosari Public Health Center and was referred to Medika Pandaan Hospital. From

Medika Pandaan Hospital, patient was diagnosed severe diphtheria and referred to

Saiful Anwar Hospital.

This case, RZ, 4-year-old boy, he was delivered spontaneously at home and

assisted by midwife. He cried soon after birth and had a bodyweight of 3100 grams and

no complication of birth. The history of the mother’s pregnancy states that during the

period of pregnancy there were no bleeding, vaginal discharge, diabetes mellitus,

drinking herbs/ medicine nor hypertension. He was the first child in the family, his

mother is 24-year-old and father is 32-year-old. His father and mother work as private.

He had breast feeding from until until the age of 15-month-old and formula milk until 2-

year-old. He was already given rice porridge at the age of 6 month and steamed rice at

2
the age of 8-month-old. As daily meals he had half plate of rice, accompanied with

meat, fish, tofu, tempe, and eggs as protein source and vegetables three times a day.

The patient was given a complete vaccination until 18 months of age, and also

diphtheria ORI on February 6th, 2018. He has a BCG scar on his right arm. His

development showed no abnormality. He could roll over and lifted his head up at 4

month, sat with assistance at 7 month, stand at 1 year, walked at 15 month, and spoke

at 18 month.

Antropometric measurements revealed he was good nutrition with body weight

was 14.5 kg (-2SD to mean), body height 97 cm (-2SD to mean) aquivalent 2-year-old,

arm circumference 14 cm (-2SD to -1SD), head circumference 52 cm (mean to 2SD)

and body weight for body height was mean.

Figure 1. From the WHO chart weight for height boys was mean.

Physical examination revealed general condition is compos mentis with sign of

heart rate was 142 beats per minutes, respiratory rate was 32 times per minutes,

temperature 38.2 °C, blood pressure 95/54 mmHg, oxygen saturation 96%. Head and

neck examination revealed edema on both neck, tender, nonerythematous, cervical

lymphadenopathy. There were found adherent membrane, greyish-white discharge on

the bilateral tonsil and larynx (figure 2). There was no conjungtivitis or secret at the

3
eyes, no secret at the ears and nostril no discharge. Chest examination showed

symmetrical chest movement, intercostal and suprasternal retraction, no rales and

wheezing. Heart sound revealed single S1, normal S2, and no murmur.

Figure 2a. Picture the patient, RZ, 4 year old boy with greyish-white membrane at
pharynx; 2b. Bullneck

Abdominal examination revealed normal bowel sounds, with unpalpable liver

and spleen. Extremities examination showed capillary refill time less than 2 second,

sensoric, and motoric system in normal limit. Deep tendon reflexes were normal.

Genetalia examination showed normal.

Complete blood count on admission (on March 9th, 2018) revealed hemoglobin

12.1 g/dl, leukocytes 11.840/ul, differential count eosinophil 0/ basophil 0.7/ neutrophil

33.2/ lymphocyte 53.2/ monocyte 12.9; it could be concluded mild lymphocytosis,

haematocrites 36.4%, thrombocytes 253.000/ul. The electrocardiography result

showed tacychardia sinus rhytm with heart rate 150 times/minute regular, there were

no prolonged P-R interval, no T-wave changes, and no dilated or hypertrophic cardiac

chamber.

4
Figure 3. The electrocardiograph showed sinus tachycardia.

Based on history taking, physical examination, laboratory, and

electrocardiography this patient was diagnosed as severe diphteria (diphteria larynx &

bullneck). Patient was diagnosed upper respiratory tract obstruction Jackson class I.

He was put on in isolation room with closed monitoring for increase severity of airway

obstruction. Nonrebreathing mask oxygen had put on this patient. Patient treated with

intramuscular Penicillin procaine dose 50.000-100.000 IU/kg per day divided two dose

to 10 days (1.450.000 IU), anti diphtheria serum 80.000 IU per intravenous (after skin

test procedure and conjungtiva test) and steroid dexametasone per injection 0.5 mg/kg

per day ( 5 mg three times per day) to 7 days and tappering off.

Second day of hospitalization (on March 10th, 2018), patient had dyspnea,

stridor and fever. The physical examination revealed increased of respiratory distress

with heart rate was 172 times/minutes, respiratory rate was 36 times/minutes,

temperature 38.5 °C, oxygen saturation 96% with nor rebreathing mask oxygen 8 liter

per minute, stidor, intercostal and suprasternal retraction. Thus, the patient

reassessment Upper Respiratory Tract Obstruction Jackson class II-III. The patient

consulted to Otolaryngology Department for tracheostomy procedure. From the

Otolaryngology collage was diagnosed Upper Respiratory Tract Obstruction Jackson II-

III e.c Larynx Diphtheria, then patient had emergency traceostomy. Post tracheostomy,

patient reffered to Pediatric Intensive Care Unit used mechanical ventilation mode

(spontan back up PEEP 5 Psupport 8 FiO2 40%), patient treated intravenous

5
midazolam continous 2 mcg/kg/minute, intravenous metylprednisolone 2 mg/kg/day,

oral N-acetylsistein 10 mg/kg/minute, periodic nebulization NaCl 0.9% and trcheal

mucous suctioning.

On the third day of hospitalization (on March 12nd, 2018), patient had

echocardiography evaluation, result showed Dilated Cardiomiophaty due to

Myocarditis. Thoart swab resulted C. Diphtheria was negative. The complain of

hoarsiness decreased and no stidor, pseudomembran at the right tonsil still looked,

overall patient in stable hemodinamic with canule trachea.

On the fifth day of hospitalization (on March 15th, 2018) patient weaned to T-

piece and on next day used masker oxygen 5 liters per minute. On the eight day of

hospitalization (on March 17th, 2018), from the physical examination, the pulse rate was

102 times per minute, the respiratory rate 22 times per minute and the body

temperature 36.8oC, electrocardiograph was normal, pseudomembran at tonsil did not

looked, patient reffered to ward.

On the sixteen day of hospitalization (on March 26th, 2018) patient’s physical

examination, had stable hemodynamics and good oxygenation so, patient done

tracheostomy decannulation.

A throat swab evaluation taken on admission to hospital was cultured. Throat

swab taken for three times on admission, 3-day, 5-day, 7-day and all results the culture

of throat swab were negative for Corynebacterium Diphteriae.

On the nineteen day of hospitalization, the last physical examination, the pulse

rate was 92 times per minute, the respiratory rate 20 times per minute and the body

temperature 36.8oC. He looked well, culture of throat for C. Diphtheriae was negative

and the electrocardiograph was normal, pseudomembran at tonsil did not looked. He

had care for 19 days and discharged with good condition.

On follow up, three weeks after the onset, there were no symptoms and signs of

peripheral neuropathy such as bilateral extremity paralysis and simetric, no complain

6
of nasal regurgitation, and dysphagia. On follow up in the second to the four week of

illness there was no tacycardia, and the electrocardiography result was normal.

DISCUSSION
In this case, the patient had dysphagia, sore throat, decreased appetite since

three days before admitted, he also suffered from moderat fever since three day before

admitted. He was confinent breath by mouth since two day before admitted, stridor,

hoarseness, and dypsnea. The neck looked swollen one day before admitted. From the

physical examination, there found neck looked edema, tender, nonerythematous,

adherent membrane, greyish-white discharge on the bilateral tonsil and larynx and it

was easy bleeds. There were no secret purulent at the eye and no konjunctivitis and no

pseudomembran at vulvovaginal and no lesion at the skin. Based on anamnesis,

physical examination and differential diagnoses include dyphtheria, infectious

mononucleosis, streptococcal tonsillitis (strep throat), and Vincent's angina.

Infectious mononucleosis (IM) or Mononucleosis syndrome is caused by an

acute infection of Epstein-Barr virus (EBV), traditionally characterized by the triad of

fever, lymphadenopathy, and pharyngitis. Fever , usually lasting 10–14 days, often

mild, especially in the last 5–7 days. Sore throat (acute pharyngitis), usually severe for

3–5 days, before resolving in the next 7–10 days. Swollen glands (lymphadenopathy),

mobile; no pain, nonerytaemotous, usually located around the back of the neck

(posterior cervical lymph nodes) and sometimes throughout the body. The most

prominent sign of the disease is often the pharyngitis, which is frequently accompanied

by enlarged tonsils with pus an exudate similar to that seen in cases of strep throat. In

about 50% of cases, small reddish-purple spots called petechiae can be seen on the

roof of the mouth. Spesific laboratory of blood showed leucocytosis and lymphocytosis.
8,9

7
 In this case, based on anamnesis the patient had fever, sore throat, swollen

neck. The physical examination, there were no enlarged tonsils with pus an exudate

but in this patient with adherent membrane, greyish-white discharge on the bilateral

tonsil, and larynx which bleeds on removal, no lymphadenopathy at posterior cervical

lymph nodes but in this patient with bullneck or swollen neck, tender, and

nonerythematous bilateral and cervical adenopathy, no petechiae on the roof of the

mouth, no skin rash, no hepatomegali and no splenomegali. The laboratory result

showed normal. So based on anamnesis, physical examination and laboratory finding

diagnose of Infectious mononucleosis can be excluded.

Strep throat is caused by group A beta-hemolytic streptococcus (GAS or S.

pyogenes). The typical symptoms of streptococcal pharyngitis are a sore throat, fever

of greater than 38 °C (100 °F), tonsillar exudates (pus on the tonsils), and large cervical

lymph nodes 30-60%. Other symptoms include: headache, nausea and vomiting,

abdominal pain, muscle pain, or a scarlatiniform rash or palatal petechiae. A throat

culture is the gold standard]for the diagnosis of streptococcal pharyngitis with a

sensitivity of 90–95%.2,10 In this case, the patiend had fever less than 38°C, no tonsillar

exudates (pus on the tonsils). Based on anamnesis and physical examination diagnose

of step throat can be excluded.

Angina vincent, this is trench mouth, a progressive painful infection with

ulceration, swelling and sloughing off of dead tissue from the mouth and throat due to

the spread of infection from the gums. Severe gingival pain, profuse gingival bleeding

that requires little or no provocation. Interdental papillae are ulcerated with necrotic

slough, other signs and symptoms may be present, but oral malodor (intraoral

halitosis), bad taste (metallic taste), malaise, fever and/or cervical lymph node

enlargement are rare.2,7 In this case, no gingival pain and bleeding, no oral halitosis, so

angina vincent can be exclude for this patient.

8
 Diphtheria has some form respiratory, cutaneus and infection at other sites.

Respiratory (nasal, pharyngeal, tinsillar and laryngeal) diphteria is typically caused by

toxin producing (toxigenic) strains of C. Diphtheriae. Cutaneus disease can cause by

either toxigenic or non toxigenic strains. Infection involved the tonsils or pharynx in

94%; the nose and larynx were the next two most common sites. After an average

incubation period of 2 to 4 days, local signs and symptoms of inflammation develop.

Fever is low-grade or absent. Infection of the anterior nares (more common in infants)

causes serosanguineous, erosive rhinitis with membrane formation. Shallow ulceration

of external nares and upper lip is characteristic. Sore throat is a universal early

symptom of tonsillar or pharyngeal diphtheria, but only 50% of patients have fever, and

fewer than 50% of patients have dysphagia, hoarseness, malaise, or headache. The

typical distinguishing features of diphtheria of the pharynx are a grey, white membrane

covering the tonsils which bleeds on removal. In previously vaccinated individuals, the

membrane may not be present.1,2,4,6

C. diphtheriae occasionally causes infections at other mucocutaneous sites

such as the ear (otitis externa), eye (purulent and ulcerative conjunctivitis involving

primarily palpebral areas), and genital tract (purulent and ulcerative vulvovaginitis).

Clinical setting, ulceration, pseudomembrane formation, and submucosal bleeding help

distinguish among other bacterial and viral causes.5,7

Patient with dyspnea, stridor and fever. The physical examination revealed sign

of heart rate was 172 beats per minutes (tacychardia), respiratory rate was 36 times

per minutes, temperature 38.5 °C, oxygen saturation 96% with Nor Rebreathing Mask

oxygen 8 liter per minutes, subcostal and intercostal retraction. The patient consulted

to Otolaryngology Department for tracheostomy procedure. From the Otolaryngologist

colleague was diagnosed Upper Respiratory Tract Obstruction Jackson class III dt.

Larynx Diphtheria, then patient had tracheostomy. Post tracheostomy, patient reffered

to Pediatric Intensive Care Unit used mechanical ventilation mode spontan back up

9
(PEEP 5 Psupport 8 FiO2 40%). Complications from diphtheria may include blocking of

the airway, damage to the heart muscle (myocarditis) apears after 10-14 day of illness,

nerve damage (polyneuropathy) apears after 3-7 week of illness, loss of the ability to

move (paralysis), lung infection (respiratory failure or pneumonia).

C.diphtheriae is not a very invasive organism, ordinarily remaining in the

superficial layers of the respiratory mucosa and skin lesions, where it can induce a mild

inflammatory reaction in the local tissue. The major virulence of C.diphtheriae results

from the action of its potent exotoxin, which inhibits protein synthesis in mammalian

cells but not in bacteria. The 62,000-dalton polypeptide toxin is composed of two

segments: B, which binds to specific receptors on susceptible cells, and A, the active

segment. After proteolytic cleavage of the bound molecule, segment A, enters the cell,

where it catalyzes inactivation of the transfer RNA (tRNA) translocase “elongation

factor 2”, present in the eukaryotic cells but not in bacteria. Loss of this enzyme

prevents the interaction of messenger RNA and tRNA stopping further addition of

amino acids to developing polypeptide chains. The toxin effects all cells in the body,

but most prominent effects are on heart (myocarditis), nerves (demyelination), and

kidneys (tubular necrosis).

Within the first few days of respiratory tract infection, toxin, elaborated locally

induces a dense necrotic coagulum composed of fibrin, leukocytes, erythrocytes, dead

respiratory epithelial cells, and organisms. Removal of this adherent gray-brown

“pseudomembrane” reveals a bleeding edematous submucosa. The membrane can be

local (tonsillar, pharyngeal, nasal) or extend widely, forming a cast of the pharynx and

tracheobronchial tree. The underlying soft tissue edema and cervical adenitis can be

intense, and, particularly in the proportionally smaller airways of children, can cause

respiratory embarrassment and a bullneck appearance. In both adults and children, a

common cause of death is suffocation after aspiration of membrane.

10
 In this patient, from echocardiography resulted early myocarditis (day-6 of

sickness). Myocarditis is inflamation of the heart muscle. Symptom can include

shortness of breath, chest pain, decreased ability to exercise, and irreguler heartbeat.

The complication may include heart failure due to dilated cardiomyopaty. Most form of

myocarditis involve the infiltration of heart tissue by one or two type proinflamatory

blood cells, lymphocytes, and macrophages plus two respective descendant of these

cells, NK cells, and macrophages which induction of diphteria toxin. Markers of

myocardial demage is troponin, in this patient the result was normal. The treatment

depend on both the severity and the cause. Medications such as ACE inhibitor, beta

blockers, and diuretics are used in this patient.

Patient had evaluation of myocarditis after 12 days of Diphtheria infection,

echocardiography resulted pericardial effusion, got medication ACE inhibitor and

echocardiography evaluation a month latter.

Subtle evidence of myocarditis can be detected in as many as two third of

patients, but 10% to 25 % develop clinical cardiac dysfunction, with risk to an individual

patient correlating directly with the extent and severity of local disease. Cardiac toxicity

can be acute, with congestive failure and circulatory collapse, or more insidious, after 1

to 2 weeks of illness with progressive dyspnea, weakness, diminished heart sounds,

cardiac dilation, and galloprhythm. Changes to electrocardiograph (ECG) pattern,

particularly ST-T wave changes and first degree heart block, can progress to more

severe forms of block, atrioventricular (AV) dissociation, and other arrhythmias, which

carry an ominous prognosis. Patients with bundle-branch blocks and complex

dissociation have a much higher incidence of death, and survivors may be left with

permanent conduction defects.

Diagnostic test for diphtheria with specimens for culture should be obtained from

nose and throat and from any affected mucocutaneous site. A portion of membrane as

well as underlying exudate should be removed and submitted for testing. Growth from

11
slants may be stained with Neisser or Loffler methylene blue and examined for

metachromatic granules. The diagnosis is made by microscopy and positive culture of

the organism from a throat swab or from tissue obtained from the inflamed

membranous area. It is important to swab beneath an edge of the membrane where

there is a higher density of bacteria.2,7 The result culture nose and throat in this case

showed negative for C. Diphtheriae.

The laboratory must be informed that diphtheria is suspected as it is not

routinely screened for. Viable organisms are not always present in culture specimens,

or are below the limit of culture detection. Consequently, molecular detection of the

diphtheria toxin gene, toxin is often the only means by which laboratory confirmation of

diphtheria can be made. The standard PCR assay that detects the C. diphtheriae tox

gene for the molecular diagnosis of diphtheria.11 In case, this results of culture C.

diphtheria were negative but PCR was not doing because we didn’t have PCR.

Principle of diphteria therapy are eradicate diphteria’s toxin, antibiotic regimen,

and supportive theraphy. Diphtherial antitoxin is the mainstay of therapy. As the

disease progresses, the efficacy of the antitoxin decreases due to its inability to

neutralise intracellular toxin.1,2,7,12,13 In this patient had given anti diphtheria serum

80.000 IU because hhe was severe diphtheria (diphtheria tonsil and bullneck), he got

ADS in the third of illness. Antibiotic therapy stops toxin production, limits the infection

and prevents transmission. Intramuscular Penicillin Procain (50.000-100.000/kg per

day divided into 2 doses) for 10-14 days.2,7,14 In this case, the patient gave penicillin

procain Intramuscularly (50.000-100.000/kg per day divided into 2 doses) ~ 725.000 IU

twice per day for 10 day. He got corticosteroid Metilprednisolone 2 mg/kg/day until 7

days and tappering off. Corticosteroid for case diphtheria in condition such as

obstruction upper respiratory tract (with or without bullneck) or in myocarditis.

Corticosteroid for this case because this is a severe diphtheria with bullneck.2,7,

12
 Strict isolation is recommended for patients with pharyngeal diphtheria. Isolation

is continued until at least two cultures from the nose and throat (and skin lesions, if

present) taken after cessation of therapy are negative. Bedrest is recommended during

the acute phase of disease.1,2,7 This patient had care in isolation room.

On the nineteen days of hospitalization, the last physical examination, the pulse

rate was 92 times per minute, the respiratory rate 24 times per minute and the body

temperature 36.8oC. She looked well, culture of nose and throat for C. Diphtheriae was

negative and the electrocardiograph was normal, There pseudomembran at tonsil was

not looked. She had hospitalization for 19 days and discharged with good condition.

Once infected, extensive peripheral tissue damage may occur due to diffusion

of the toxin through the body. The heart and central nervous system are targeted.

Myocarditis and neuritis can occur in the first week. Most often, first evidence of

cardiomyopathy is recognized in the second to third week of illness as pharyngeal

disease improves, but it can appear as early as the first week (when fatal outcome is

high) or insidiously as late as the sixth week of illness. Tachycardia out of proportion to

fever is common evidence of cardiac toxicity or autonomic nervous system dysfunction.

Prolonged P-R interval or ST-segment and T-wave changes are relatively frequent

findings on electrocardiogram, and dilated or hypertrophic cardiomyopathy is frequently

observed on echocardiogram. Single or progressive cardiac arrhythmias can occur,

such as first-, second-, and third-degree heart block, atrioventricular dissociation, and

ventricular tachycardia.1,2,15 In this patient no sign and symptom suggest myocarditis

from echocardiography on third day of hospitalization, and from the serial

electrocardiography showed normal result.

Neurologic complications also parallel the extent of primary infection and are

multiphasic in onset. Six to seven weeks after onset of oropharyngeal inflammation,

hypoesthesia and local paralysis of soft palate commonly occur. Weakness of posterior

pharyngeal, laryngeal, and facial nerves may follow, causing a nasal quality in voice,

13
difficulty in swallowing, and risk of death from aspiration. Cranial neuropathies usually

occur in the fifth week, leading to oculomotor and ciliary paralysis, manifested as

strabismus, blurred vision, or difficulty with accommodation. Symmetric polyneuropathy

can have its onset 10 days to 3 months after onset of oropharyngeal infection and

principally causes motor defect and diminished deep tendon reflexes.1,2,3 In this

patient, there were no symptoms, signs and physical examination suggesting

peripheral neuropathy.

For this case-patient, he was 4 years old, he got complete immunization. This

patient plan to given Td vaccine at 4 weeks after hospitalization.

Immunity to diphtheria can measure with Schick test. The Schick test, is a test

used to determine whether or not a person is susceptible to diphtheria. A positive

reaction occurs in individual without toxin-neutralizing antibodies.1,18,19 In this case,

Schick test not doing to this patient because we didn’t have reagen.

In this case, complete immunization status in this patient can not be correlated

severity degree of the disease. Prevention to diphtheria with vaccination DPT. There

was significant effectivity immunization, reported person who got immunization only

occur mild infection 81,3%, moderate infection 16,4% and severe infection only 2,3%.

But person who didn’t given immunization occur severe infection 59,5%, moderat

infection 21,5% and mild infection 19%.20

The right of medication administration should be applied in vaccine

administration are the rigth patient, the right vaccine or diluent, the right time, the right

dosage, the raight route, needle lenght, and technique, the right site, and the right

documentation (including the administration of vaccines at the correct age, the correct

distance interval time and the expired of the vaccine and its dilution). One of the most

important is vaccine storage and cold chain management. Cold chain is a network of

refigerators, cold stores, freezers and cold boxes organised and maintained so that

14
vaccine are kept at the right temperature to remain potent during vaccine tranportation,

storage and distribution from factory to the point of use.23

The vaccines must be kept at the correct temperature when being transported.

Maintenance of the cold chain requires vaccines and diluents to be, collected from an

airport as soon as they arrive, transported at the correct temperature from the airport

and from one store to another, stored at the correct temperature in stores at the

provincial, county, city, township or village health centres, transported at the correct

temperature to outreach sites, and
 kept cold during immunization sessions or

rounds.24

From a logistics point of view, the same principles of distribution apply as in

general logistics distribution. These principles are covered in the Distri bution topic with

the exception of the use of specialised carriers and containers as discussed in this

topic. The distribution of cold chain should be built into the organizational distribution

plan to maximize on the limited transport facilities available during emergencies. In the

cold chain the logistician must pay particular attention to the vaccine arrival and

temperature control.23

Every international shipment of vaccines from a manufacturer should include a

blank vaccine arrival report (VAR) form, as shown on the following page. When the

shipment arrives, the individual responsible for monitoring vaccine arrivals and storage

fills in the VAR and gives a copy to the local office of the procuring agency. The report

documents the condition of the shipment and the quantities received, and it confirms

that all other necessary documentation is included. If problems occur, the VAR can be

the basis for initiating corrective action or making claims.23

Vaccine Arrival Report (WHO/UNICEF) The logistics function must avoid:

shipment of vaccines by way of airports that lack cold rooms, consignments to the

wrong party, shipment of the wrong vial sizes, shipment of the wrong quantity of

vaccines and diluents, shipment of vaccines that are due to expire soon, arrival of

15
vaccines on weekends or holidays, shipment of vaccines without : (advance

notification
 , sufficient icepacks
 , cold chain monitors
 , documentation needed for

customs clearance (Taken from Immunization Essentials – A Practical Field Guide,

USAID, 2003)).

The organisation of supply within a country is an integral part of the overall cold

chain system, and should be properly planned and executed. There are two types of

supply procedures: vaccines and other supplies to be collected by lower level

institutions, and supplies to be delivered to the lower level institutions. See

Organisation of Vaccine supply for details.23

Some vaccines are very resistant to heat and are shipped from the

manufacturer without insulation. They are, however, damaged by temperatures above

+48°C. A special device is therefore used to monitor temperatures during shipment.

One indicator is included with each shipment of minimum doses. The shipping indicator

should be kept with vaccines if they have to be stored outside the cold chain.

In cold climates, vaccines should be protected from freezing during transport.

They should therefore be packed with a cold-chain monitor and Freeze Watch TM,

according to the procedures. To avoid damage to the vaccines the staff must know how

temperatures are monitored and understand how to interpret temperature readings

(indexes).23

Table 1. Recommended temperature ranges

Stages of the Maximum Minimum

Vaccines
cold chain temperatures temperatures

OPV, BCG, measles, yellow

All + 8°C -20°C
fever

Hepatitis B, DTP All + 8°C + 2°C

DT, TT Transport + 40°C + 2°C

DT, TT Storage + 8°C + 2°C

16
 Diluent Transport Ambient + 2°C

Diluent Storage Ambient + 2°C

Diluent Point of Use + 8°C + 2°C

Managenent for asimptomatic carrier, when an asymptomatic carrier is

identified, the following steps should be taken:

1. Give antimicrobial prophylaxis for 7 to 10 days.

2. Give age-appropriate preparation of diphtheria toxoid immediately if the individual

has not received a booster within 1 year.

3. Place individuals in strict isolation (respiratory tract colonization) or contact isolation

(cutaneous colonization only) until at least two subsequent cultures taken at least 24

hours apart after cessation of therapy are negative for C. diphtheriae.

4. Perform repeat cultures at a minimum of 2 weeks after completion of therapy in

cases and carriers, and, if cultures are positive, an additional 10-day course of oral

erythromycin should be given and follow-up cultures performed.2,7

SUMMARY

We have been discuss case of severe diphtheria in a boy 4 years old. The

diagnosis achieved by trough history taking, physical examintaion and laboratories

culture throat swab for C. Diphtheria. These patient had complete imunization since

birth but why patient still suffer from diphtheria. One of the risk factor maybe from

vaccine administration. The treatment for severe diphtheria were anti diphtheria serum,

antibiotic penicillin procain, corticosteroid and tracheostomy.

17
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