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Summary Pediatric communicable diseases-2 mind map

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clear and structured mind map that summarizes the most important pediatric communicable diseases in a visually organized layout. It highlights key infections in children, including their causes, transmission routes, clinical features, complications, and basic prevention strategies. The map simplifies complex pediatric infectious diseases into easy-to-follow branches that support fast learning and long-term memory

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Infectivity Clinical manifestations: clinical manifestation Complications: diagnosis Treatment
The incubation period is around 10-21 days.
The prodromal period: Prodromal symptoms may be present, particularly in older children. Fever, malaise, anorexia, Progressive Varicella:
Etiology: headache, and occasionally mild abdominal pain may occur 24-48 hours before the rash appears. with visceral organ involvement, coagulopathy, severe Children receiving long-term corticosteroids and/or immuno-suppressive drugs are
The etiological agent is the same for chickenpox and herpes zoster which is one of the herpes group, called Varicella zoster virus (VZV). An Exanthema: In children it begins the illness. In babies only may be seen few vesicles. In older children the rule is a profuse rash.
If the prodromal period is evident then the disease is expected to besevere.
hemorrhage, and continued lesion development is a dreaded
complication of primary VZV infection. Severe abdominal pain 🔹
at risk of severe, often fatal, chickenpox.
Secondary bacterial infection of the skin: Most common one. May cause
important characteristic of the whole herpes group is that they causes
🔹
The rash: The rash has several characteristics as follows: and the appearance of hemorrhagic vesicles in otherwise healthy overwhelming streptococcal/staphylococcal generalized sepsis among some cases
🔹
Diagnosis: Laboratory tests are rarely needed.

🔹 Leucopenia, relative lymphocytosis, normal ESR.
(i) primary infection, (ii) latent infection, and (iii) reactivated infection (s).
🔹
The stages are: macules, papules, early and late vesicles, pustules, and crusts or scabs. Mainlythe vesicles, pustules, and
crusts are detected but the others are not seen usually.
adolescents and adults, immunocompromised children, pregnant

🔹 🔹
of chickenpox.
The virus can be identified quickly by direct fluorescence assay (DFA) of cells from
🔹
The primary infection (in this case chickenpox). The virus establishes latent infection in sensory nerveganglia; its reactivation after variable women, and newborns may herald this. Thrombocytopenia: Causes hemorrhagic chickenpox with bleeding in vesicles. Mostly is symptomatic.
cutaneous lesions, which is widely available, and by polymerase chain reaction (PCR)
time (usually many years) by herpes zoster. It is stated that lifetime risk of having zoster is around 20-30%.
🔹
It begins as crops for 2-3 days, and polymorphic thus are seen several different lesions in the same time (vesicles, pustules,
and crusts)
Varicella bullosa: Uncommon. Possibly related to
🔹
Sudden onset in the in 2nd or 3rd day of rash and rapid deterioration. May respond

🔹
amplification testing. Although multinucleated giant cells can be detected from scraping
🔹 For itching soothing ointments or calamine lotion; antihistamines also can be used.

🔹
staphylococcal superinfection. Is to be treated by an appropriate dramatically to systemic corticosteroids. Gurgling with oral antiseptic fluids after the food intake.
CHICKENPOX Epidemiology:
Varicella is highly contagious. It is less contagious than measles, but more so than mumps and rubella. Around 90% of the patients are below
It is infective from 24-48 hours before the
appearance of the rash until all the lesions are 🔹 Lesions are superficial, seeming like drops of water, especially the vesicles.
Varicella lesions often appear first on the scalp, face, or trunk, covering almost all regions of the body, even may appear on 🔹
anti-staphylococcal antibiotic.
Varicella gangrenosa: Rare. May be due to secondary
Pneumonia: Rare. May occur in neonates or adults (two extremes) with severe
manifestations that may be fatal. 🔹
the floor of fresh vesicle.
VZV immunoglobulin G (IgG) antibodies can be detected by several methods and a 4-
fold rise in IgG antibodies is also confirmatory of acute infection.
Treatment with antivirals is not routinely recommended for otherwise healthy children with varicella. Antiviral agents (acyclovir) can be tried
early (the first 48- 72 hours of illness) especially in high-risk groups or with severe illness.
(Varicella) 10 years. The peak age is between 5 and 9 years, though it occurs at any age, including neonates. Varicella is a more serious disease in young crusted; around 3-7 days.
🔹
palms and soles, though this latter form is not so common.
The distribution of rash is typically CENTRIPETAL i.e. seeking the center of the body. In other words, lesions are more
bacterial infection.Lesions become necrotic forming a dense
black scar which may extend down to the muscular layer. May 🔹
Central nervous system:
Encephalitis: Not frequent. More observed in children than adults. Usually is
Differential diagnosis: 🔻 Prevention: Vaccination (live attenuated virus) is applied routinely in many countries. Passive immunization with Zoster Immune Globulin
infants, adults, and immunocompromised persons, in whom there are higher rates of complications and deaths than in healthy children. Within
households, transmission of VZV to susceptible individuals occurs at a rate of 65-86%. Second attacks may occur, though uncommonly. In
concentrated nearer to the center of the body e.g. greatest concentration of lesions on the trunk, fewest lesions on the distal

🔹
extremities. 🔹
have a fatal outcome.
Congenital and neonatal varicella: Transplacental passage 🔹
acute with a very common cerebellar ataxic form.
Other neurological complications: Guillain-Barre' syndrome; transverse Includes vesicular rashes caused by other infectious agents, such as herpes simplex virus,
scabies, or impetigo; drug reactions; contact dermatitis; and insect bites. Severe varicella
(ZIG) can be given for high-risk patients once they are incontact with an infectious individual, or utmost within 72 hours of exposure. This
measure can prevent/attenuate the illness.
adults second attacks take the form of herpes zoster.
Spread: 🔹
Rash tends to come out in hollows and protected parts of the body, rather than on the prominent and exposed areas e.g.
between scapulae more than over them.
of the virus from an infected pregnant mother may cause:
Congenital form: If the passage occurred carly then is likely to 🔹
myelitis; optic neuritis.
Reye syndrome: especially in cases taking aspirin with varicella. Around 10% of was the most common illness confused with smallpox before the eradication of this
disease.
It is spread by direct contact with skin lesions (vesicles, not the crusts) and/or airbome droplets from naso-pharyngeal secretions (acquired). 🔹
🔹
Pruritus is prominent causing rupture and often superinfection of lesions.
Fever usually is low-grade, rarely the fever as high as 40°C with little malaise and a mild sorethroat.
Mucous membranes may be involved. Ulcerative lesions involving the oropharynx and vaginaare also common; many
cause some malformations, especially involving the limbs and the
CNS e.g. hemimelia. If passage occurred late then a neonatal form 🔹
Reye syndrome cases had chickenpox.
Rare complications: Nephritis, nephrotic syndrome, hemolytic-uremic syndrome,
arthritis, myocarditis, pericarditis, pancreatitis, orchitis, uveitis, iritis, and hepatitis.
is more likely that may be severe with a case fatality of around
In utero infection can also occur as a result of transplacental passage of virus during maternal varicella infection.
🔹
children have vesicular lesions on the eyelids and conjunctivae, but corneal involvement and serious ocular disease is rare.
The rash rarely to be hemorraghic
20-30%.



🔻 Treatment:

🔹
Early treatment of pertussis is very important. The earlier a person, especially an infant, starts treatment the better.
Goals of therapy are to limit the number of paroxysms, to observe the severity of the cough, to provide assistance when necessary and to

Pertussis (whooping cough) is an important cause of infant death worldwide and continues to be a public health concern even in countries The incubation period is usually between 3-12 days. There are three distinct stages:
🔹
educate parents in the natural history of the disease and in care that will be given at home.
Infants 3 months of age are admitted to hospital almost without exception, as are those between 3-6 months unless witnessed paroxysms
are not severe, and those of any age if significant complications occur. Prematurely born young infants and children with underlyingcardiac,
with high vaccination coverage. 1. Catarrhal stage: pulmonary, muscular, or neurologic disorders have a high risk for severe disease.
Etiology: Usually epidemic whooping cough is caused by Bordetella pertussis. Less frequently is caused by B.parapertussis. Bordetellae are
🔹
that lasts 1-2 weeks. Is characterized by:
🔹
I-General measures:
🔹
gram negative rods requiring special media for culture and prompt culturing or strict preservation prior to culture, otherwise they die out Non distinctive symptoms of congestion and rhinorrhea variably accompanied by low-grade fever, sneezing, lacrimation, Complications:
rapidly. For this reason, Bordetellae are infrequently cultured in many laboratories. The mentioned causative agents are undistinguished
conjunctival suffusion, and a mild cough (all similar symptoms to the common cold). As initial symptoms wane, coughing
marks the onset of the paroxysmal stage.
Respiratory: Otitis media especially in young children and
infants.Bronchopneumonia: Is a serious complication. When it occurs often the
Diagnosis:
Clinical diagnosis is easy in the presence of an epidemic among children. It is difficult early 🔹
🔹
Avoidance of factors that provoke cough
Appropriate nursing care
Attention to nutritional state; oral, nasogastric or parenteral nutrition may be recommended.
2. Paroxysmal (spasmodic) stage: in the illness (nonspecific manifestations).
🔹
spasmodic cough ceases temporarily. Once improvement supervenes reappears the - Mist by tent can be useful in some infants with thick, tenacious secretions and excessively irritable airways.
Likewise, it is difficult among older children and adults for the atypical presentation.
morphologically, being differentiated by culture and specific agglutination reactions. They have no cross immunity. Infectivity: 🔹
Lasts around 2-6 weeks and is characterized by: Intense, irritating cough that occurs in bouts (attacks) In infants 3 months of age may have complete apnea at the
🔹
characteristic cough.
🔹
Paraclinically: II- :Early antibiotic therapy
🔹
Each bout consists of several coughs that occur in a single expiration, air being forced out with each cough leaving at the end of the bout, becoming deeply cyanosed (almost black lips) Bronchiectasis, atelectasis. TB reactivation: is reported by a few authors.
Epidemiology: There are 60 million cases of pertussis a year occur worldwide, resulting in more than 500,000 deaths. Widespread use of Patients are infective from onset of the end a very small amount in the lungs. At the end of the bout, more air than normal rushes in through the almost closed glottis Pressure effect: With the continuous cough the intrathoracic pressure increases Leukocytosis (15,000-100,000 cells/mm3) due to absolute lymphocytosis is may help to reduce the severity of infection but, for sure decreases the infectivity period of the cases thus rendering them non- infectious for
and in the worst of cases, convulsions may occur. At this stage of others, even if the course and severity might not be affected especially if diagnosis was not made so early. Macrolides are preferred agents.
pertussis vaccine led to a greater than 99% decline in cases. Highest risk is found among those under 5 years of age. At all age-groups
females are more commonly affected than males, a difference with almost all infectious diseases (male predominance). Infants have the
manifestations to up to 3 months, if left
untreated.Neither natural disease nor vaccination 🔹
thus giving rise to the characteristic whoop.
Initially, the child's face becomes congested. red. but as coughing increases (no pause for breath), cheeks change to blue,
apnea the cord relaxes, and then the infant gasps and without
any whoop the air flows into the lungs, acquiring newly a normal
thus predisposing to a group of complications as: Petechiae on the head and neck;
subconjunctival hemorrhage; rarely, intracranial hemorrhage; umbilical or inguinal 🔹
characteristic in the catarrhal stage,
The culture is cumbersome and needs a very cautious manipulation of the specimen as Erythromycin (oral) in a dose of 40-50 mg/kg/24hrs in four doses for 10 to 14 days. Azithromycin 10 mg/kg/day in a single dose for 5 days.
Other macrolides (clarithromycin 15 mg/kg in2 divided doses for 7 days) may be of help but expensive. The Co-trimoxazole is mentioned, by
PERTUSSIS provides complete or lifelong immunity against eyes bulge, veins of the scalp and neck engorge, with tearing and salivation, and the tongue is protruded. After the whoop, the Bordetellae readily die outside a favourable media. However, culture remains the gold
🔹
highest morbidity associated with pertussis, although adolescents and adults now account for the majority (67%) of reported cases as skin color. He (she) may then go in a sleep. herniae and rectal prolapse; pneumothorax, pneumomediastinum, subcutaneous some authors, as an alternative for erythromycin in patients who are allergic to macrolides.
vaccine-induced immunity wanes and they become susceptible to infection.
reinfection or disease.
Therefore, many newborns (small infants) are 🔹
normal color is regained if no new bout is to occur.
The number of coughs in each attack is variable according to severity from 5 to around 30, while in mild forms five attacks
In Adolescents and previously immunized children: the whoop
may be absent probably because of a wider stronger air 🔹
emphysema; rarely diaphragmatic rupture.
Neurological: Convulsions: Are usually a result of hypoxemia, particularly 🔹
standard for diagnosis.
Other investigations that are helpful for diagnosis but are still not standardized include
the fluorescent antibody tests, specific antibodies (IgA, IgG etc), and PCR.
III- Pertussis immunoglobulin:
No documented benefit. Very scanty reports mention it as valuable.
likely to be susceptible and catch the infection.
Pertussis is one of the most contagious diseases. It is considered to beendemic in many communities, with superimposed epidemics that occur Parapertussis may cause similar, but milder, 🔹
may be reported in a day.

🔹
passages.* among small infants, but hyponatremia from excessive secretion of antidiuretic IV- Antitussive: No clear-cut benefit but are always tried, mostly for social reasons!!!
🔹
every 3-5 years. It occurs more commonly from July through October, with attack rates as high as 100% in susceptible individuals exposed to The child may expel some thick sticky mucus at the end of the bout. May vomit and then sinks back asleep from exhaustion. 3. Convalescence (22 wks): the number, severity, and duration hormone during pneumoniacan occur. V. Isolation: Patients with suspected pertussis are placed in respiratory isolation with use of masks byall health care personnel entering the
illness. Differential diagnosis:
🔹
Frequently, he (she) passes into another fit of coughing, perhaps several times before relief. Inbetween the attacks the child of episodes diminish May have, as sequels, paralysis (hemiplegia), deafness, blindness, aphasia, etc. room. Patients are placed in respiratory isolation for 25 days after initiation of erythromycin therapy. Children and staff with pertussis in child
aerosol droplets at close range. Neither natural disease nor vaccination provides complete or lifelong immunity against reinfection or disease. Protracted cough can be caused by Mycoplasma, parainfluenza, enteroviruses,RSV, or
Protection against typical disease wane 3-5 years after vaccination unmeasurable after 12 years. 🔹
looks healthy.

🔹
Gastrointestinal: Mouth ulceration is a frequent complication especially of the
adenoviruses. Other causes respiratory allergy, bronchial asthma, foreign bodies, etc. care facilities or schools should be excluded until erythromycin has been taken for 5 days.
🔹
Physical examination reveals no outstanding findings. frenulum linguae. VI- Other therapies: A handful of small clinical trials and reports suggest a modest reduction of symptoms from the ẞ2-adrenergic stimulant
Pertussis-like syndrome may simulate whooping cough of may be included here at the top
Subclinical reinfection undoubtedly has contributed significantly to immunity against disease ascribed previously to both vaccine and prior 🔹 Fever is not an important feature in the uncomplicated cases*
The first two weeks are the most distressing. The slightest disturbance, emotional or physical, may throw the patient into a
Malnutrition: Pertussis interferes with infant's ability to feed, and due to
prolonged duration ofillness. of diseases to be differentiated. salbutamol (albuterol).
infection. B. pertussis does not survive for prolonged periods in the environment.
Spread: The main source are the nasopharyngeal droplets spread through intense coughing, sneezing etc. Close contact is the main way of 🔹
spasm. 🔻 Prevention: By active immunization (using the "pentavalent" vaccine) as scheduled. A new one, the acellular vaccine (DTaP), that seems to be

transmission. Older children and adults may have subclinical or mildly presented infections which are undiagnosed and form a great source 🔹 The nutritional status may be adversely affected by these bouts of cough and vomiting. more effective and less reactogenic, DTaP vaccines have fewer adverse effects than the vaccines containing whole-cell pertussis (DTP). which

of spread among other susceptible individuals, especially in endemic areas. 🔹
continues to be given to infants and children in many other countries.
Care of Househoid and Other Close Contacts:
Contacts of a case must be given a macrolide agent: the same age-related drugs and doses for prophylaxis are used for treatment. Visitation
and movement of coughing family members in the hospital must be assiduously controlled until erythromycin bas been taken for 5 days. If age
is below 7years a booster of DPT can be given unless it was given during the last 6 months.



🔻 Treatment:

communicable Tetanus, historically called lockjaw, is spastic paralytic illness caused by tetanus toxin produced by the vegetative form of Clostridium tetani
The objectives of treatment are: eradication of C. tetani and the wound environment conducive to its anaerobic multiplication, neutralization of
all accessible tetanus toxin, control of seizures and respiration, palliation and provision of meticulous supportive care, and, finally, prevention
of recurrences.

diseases 2 at an injury site, causes illness through the effects of a singletoxin, tetanospasmin. - Admitted the patient in a quiet, dark room, by protected from all unnecessary sounds, sights and touch with adequate nursing care.
Specific treatment:
Etiology: The incubation period is of 3-14 days, but it may be as long as months after the injury (N.B. dormant spores).
Cl.tetani is an obligate anaerobic, gram positive, non-encapsulated, motile bacilli that form terminal spores resembling drum sticks. It exists in There are two major typical features of tetanus: 1. Tetanus antitoxin (TAT) or human Tetanus immunoglobulin (TIG): the TAT is the available here and can be given in a dose of 10000 U
two forms: vegetative (susceptible to heat and many adverse conditions), and spores (highly resistant to many adverse conditions). The muscle rigidity and muscle spasm. after a test dose in single IV/IM injection, whatever is the age of the patient (even for adults!!!). Desensitize if hypersensitive. The TIG is actually
The rigidity is manifested by persistent contracture of a group of muscles either in a generalized form (masseter, abdominal, the first choice treatment of tetanus but is not available here.
Spread: spinal and limb muscles) or as a localized to a few muscles. Once develops the rigidity is continuous throughout the illness. Can be given in a single dose of 500 U. Is given only IM with no need for a test dose.
The spores survive in soil for years and may be found in house dust and feces of animals and humans. Muscles involved can be assessed by palpation, being hypertonic. The spasms are characterized by intermittent intense Many authors put a very high dose for both TAT and TIG whichis just thrown away as the amount of free toxin is very low, and the stated doses
contraction that occurs in response to any stimuli(visual, auditory, or tactile) at intervals that vary according to severity of the are just enough for treatinent of tetanus, particularly when speaking about patients that are usually from poor socio-economic stratum who
illness. must pay for the treatment.
Epidemiology: Forms: 2. The wound must be cleansed and debrided (can be postponed till patient is sedated and antitoxin administered). Excision of the umbilical
Tetanus occurs worldwide and is endemic in approximately 90 developing countries. The most common form, neonatal (or umbilical) tetanus, Tetanus may be either generalized, which is more common, or localized. Complications: stump in neonatal tetanus is no longer recommended.
kills approximately 500,000 infants each year, with about 80% of deaths in just 12 tropical Asian and African countries. In addition, an 1. Generalized tetanus: - Aspiration of secretions and pneumonia. 3. Antibiotics: Metronidazole oral or intervenous 30 mg/kg per day, given at 6- hour interval remains the antibiotic of choice. Penicillin G
- The first sign is trismus (masseter muscle spasm, or lockjaw), is found in more than half of the cases, at the onset. (100,000 U/kg/day dividedevery 4-6 hr IV is an alternative treatment. Antimicrobial therapy duration 7-10days.
estimated 15,000-30,000 unimmunized women worldwide die each year of maternal tetanus, which results from postpartum, postabortal, or - Shortly the rigidity spreads to other major groups of muscles causing dysphagia, neck stiffness, abdorninal rigidity, and 2. Localized tetanus results in painful spasms of the muscles
- Maintaining airway patency often mandates endotracheal intubation and
Diagnosis: 4. All patients with generalized tetanus need muscle relaxants. Diazepan provides both relaxation and seizure control; the initial dose of
mechanical ventilation with their attendant hazards, including pneumothorax and
postsurgical wound infection with C. tetani. opisthotonus, i.e. contracted back, abdomen, neck and lowerlimbs. adjacent to the wound site and may precede generalized tetanus, mediastinal emphysema. The diagnosis may be established clinically. 0.1-0.2 mg/kg q 3-6 hrs given intravenously is then titrated to control the tetanic spasms, after which it is sustained for 2-6 wk before its

TETANUS
Most non-neonatal cases of tetanus are associated with a traumatic injury, often a penetrating wound inflicted bya dirty object such as a nail, - Spasm of the facial muscles is manifested as Risus sardonicus. but is generally milder. - The seizures may result in lacerations of the mouth or tongue, in intramuscular The typical setting is an unimmunized patient(and/or mother) who was injured or born tapered withdrawal. Magnesium sulfate, other benzodiazepines (e.g., midazolam), chlorpromazine, dantrolene, and baclofen are also used.
- Tetanic seizures are characterized by sudden burst of spasms of various muscles, flexion and adduction of the upper limbs, within the preceding 2 weeks and who presents with trismus,other rigid muscles, and a Baclofen should be used only in an intensive care unit setting. The highest survival rates in generalized tetanus are achieved with
splinter, fragment of glass, or unsterile injection, infected animal bites. Infectivity: 2.1 Cephalic tetanus is a rare form of localized tetanus involving
hematomas or rhabdomyolysis with myoglobinuria and renal failure, or in long bone
clear sensorium. C. tetani is not always visible on Gram stain of wound material, and it is neuromuscular blocking agents such as vecuronium and pancuronium. Autonomic instability is regulated with standard a and ẞ or (both)
clenching of fists and extension of the lower limbs. or spinal fractures.
The route of entry are the contaminated wounds especially the dirty, necrotic wounds; suppurating umbilical stump; but, not infrequently, in Tetanus is not contagious from person to person.

(Lockjaw)
- Initially these spasms occur for seconds, later on minutes separated by periods of relative relaxation, in presence of the the bulbar musculature that occurs with wounds or foreign - Venous thrombosis, pulmonary embolism, gastric ulceration with or without isolated in only about 30% of cases. blocking agents; morphine has also proved useful.
It is vaccine- preventable disease
absence of any apparent focus, or after the most trivial and innocent wound. No age is immune, unless well supported by immunization. rigidity which continues throughout the active illness. bodies in the head, nostrils, or face. It also occurs in association hemorrhage, paralytic ileus, and decubitus ulceration are constant hazards. 5. The ideal treatment for severe spasms and contractions is by means of muscle paralysis and mechanical respiration via endotracheal
Well-protected pregnant mothers can afford protecting immunoglobulins to the offspring, which will be born with some transient immunity - Spasms may be precipitated by visual, auditory, or tactile stimuli. with chronic otitis media. Cephalic tetanus is characterized by - Cardiac arrhythmias, including asystole, unstable blood pressure, and labile Differential diagnosis: Trismus may result from para pharyngeal, retropharyngeal, or tube in an ICU. Tracheotomy may be needed.
- The patient is completely conscious) during the spasm and usually is apprehensive, afraid of the spasms. retracted eyelids, deviated gaze, trismus, risus sardonicus, and - temperature regulation reflect disordered autonomic nervous system control that dental abscesses, or rarely, from acute encephalitis involving the brainstem. Other include: 6. Prophylactic subcutaneous heparin may be of value.
against tetanus. - The spasms of the respiratory muscles may cause respiratory obstruction, cyanosis and death. spastic paralysis of tongue and pharyngeal musculature. may be aggravated by inattention to maintenance of intravascular volume needs. rabies, hypocalcemia, epileptic seizures, narcotic withdrawal etc. 7. After the patient has improved the vaccination against tetanus is to be administered by means of tetanus toxoid as the disease provokes no
Tetanus infection gives no immunity, so those survivors need to beimmunized against tetanus. - The manifestations may increase over 3-7 days, plateau during the 2nd week and abate gradually in 2-4 weeks. - ✓ Sequels: There is no permanent organic sequel unless a spinal fracture occurs, immunity.

Pathogenesis:
- There may be associated fever, or hypothermia, sweating, cardiac arrhythmia, etc
Neonatal tetanus (tetanus neonatorum):
which is very rare.
🔻 PreventionTetanus

The disease will not develop unless spores change to vegetative (active) forms under favorable (anaerobic) local conditions produce the
3 to 10 days after birth. It results from unclean delivery and unhygienic management of the umbilical cord in an infant born to a
🔹
is an entirely preventable disease.

🔹
mother who has not been iminunized against tetanus, or circumcision with a contaminated blade startsthis form Active immunization
toxins (tetanospasmin and tetanolysin). In the occasional cases of no apparent portal of entry, is presumed that spores previously introduced Is a generalized one, mainly characterized by progressive difficulty in sucking and swallowing, with associated hunger and with tetanus toxoid (T_T) IM either mixed in Pentavalent or DT. Now, is recommended the combined Td for adults instead of the TT. Immunization
in the skin remained dormant in tissue for long time and germinated (to vegetative forms) when conditions became favorable (anaerobic)
causing the illness. Toxins reach the CNS through nerves and/or blood.
🔹
crying.
Paralysis or diminished movement, stiffness to the touch, and spasms, with or without opisthotonos, characterize the 🔹
of women at least 2 doses with tetanus toxoid prevents neonatal tetanus.
Wound Management:

🔹
disease. It depends on nature of injury and the immunization state of the patient.
They interfere with neuromuscular transmission and suppress the inhibitory influences on motor neurons, which lead to hypertonicity, spasms, The umbilical stump may hold remnants of dirt, dung, clotted blood, or serum, or it may appear relatively benign. - The wound should be cleansing carefully, and to remove foreign bodies and any necrotic tissue in which anaerobic conditions might develop.
- In any other circumstance e.g. patients with an unknown or incomplete immunization history; affected by a possible tetanigenic wound a
and seizures. booster dose of the Tetanus toxoid should be givento stimulate active immunity. TIG in a dose 250-500 U IM should be given, if not available
Also. lead to a fluctuating overactivity of the sympathetic nervous system (tachycardia, labile hypertension, cardiac arrhythmia, peripheral TAT of 3,000-5,000 U may be
vasoconstriction, profuse sweating.. etc.). - given IM after test dose. If fully immunized nor TIG or TAT is indicated.
A booster of Tetanus toxoid is administered to injured persons who have completed the primary immunization series if
Toxins bound to tissue are not dissociated nor neutralized by antitoxin. (1) the wound is clean and minor but ≥10 yr have passed since the last booster or
(2) the wound is more serious and 25 yr have passed since the last booster.



Clinical features
Diphtheria is an acute toxic infection caused by Corynebacterium species, typically Corynebacterium diphtheria it is aerobic, After an average incubation period of 2-4 days, local signs and symptoms of inflammation develop. The manifestations of C.
nonencapsulated, non-spore-forming, mostly nonmotile, pleomorphic, gram-positive bacilli. diphtheriae infection are influenced Complications:
Epidemiology: diphtheria remains endemic in many developing countries with poor immunization rates against diphtheria.it primarily affected
children <15 years of age.
by the anatomic site of infection, the immune status of the host, and the production and systemic distribution of toxin. More
than one anatomic site may be involved simultaneously. The most important forms are:
(i) Toxic cardiomyopathy:
Toxic cardiomyopathy occurs in approximately 10-25% of patients with diphtheria 🔻
🔻 Treatment

Spread: C. diphtheriae is an exclusive inhabitant of human mucous membranes and skin.
Respiratory diphtheria:
The primary focus of infection was the tonsils or pharynx in 94%, with the nose and larynx being the next two most common
and is responsible for 50-60% of deaths. 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
Diagnosis:
Clinical diagnosis is possible in areas with endemic disease, but may be difficult in non-
🔹 Supportive care:
Once diagnosed a patient must be kept in complete bed rest is essential, during the acute phase of disease, usually for 2 wk until the risk for
symptomatic cardiac damage has passed, with a return to physical activity guided by the degree of toxicity and cardiac involvement. Also for
Spread is primarily by airborne respiratory droplets, direct contact with respiratory secretions of symptomatic individuals, or exudate from
infected skin lesions. Asymptomatic respiratory tract carriage is important in transmission. Organisms can remain viable in dust or on fomites 🔹
sites.
Nasal: Infection of the anterior nares, is more common among infants, causes serosanguineous, purulent, erosive rhinitis system dysfunction
- Dilated and hypertrophic cardiomyopathy. Cardiac dysrhythmias can occur.
endemic regions. However, once a peculiar picture of chronic wounds, nasal affection with
muco-bloody secretions, severe cervical lymphadenitis with extreme toxicity and 🔹
such cases are needed frequent ECGs i.e. 2-3 times per week, for the first few weeks.
Hydration must be cautiously calculated taking in account the CVS status and other clinical parameters as intake and losses etc.-
for up to 6 mo. 🔹
with membrane formation. Shallow ulceration of the external nares and upper lip is characteristic.
Tonsillar and pharyngeal: Sore throat is a universal early symptom, but only half of patients have fever, and fewer have - Clinical congestive heart failure. exudative tonsillitis (uni or bilateral) that bleeds easily upon trying to remove its exudates
etc. one may investigate a probable diphtheria. 🔹
Nutritional support is indicated by NGT or parenterally.
Transmission through contaminated milk and an infected food handler has been proven or suspected. dysphagia, hoarseness, malaise, or headache. Mild pharyngeal injection is followed by unilateral or bilateral tonsillar - Recovery from cardiomyopathy is usually complete, although survivors of more
severe dysrhythmias can have permanent conduction defects. Paraclinically: 🔻 Cutaneous wounds are cleaned thoroughly with soap and water.

🔹 Antitoxin: Must be used as early as possible, intravenously after test dose is needed as serum is derived from animals. Antitoxin is
Specific:
DIPHTHERIA The immunity is gained by means of adequate immunization. Natural infection is said to cause some immunity in around 50% of the cases, membrane formation, which extends variably to affect the uvula, soft palate, posterior oropharynx, hypopharynx, and glottic Depend on clinical picture and culture obtained from the nose and throat and any other
areas. (ii) Toxic neuropathy:
mucocutaneous lesion. Culture is important to determine the presence of the
thus it is mandatory to vaccinate those affected. Underlying soft tissue edema and enlarged lymph nodes can cause a bull-neck appearance. The paralysis is the main CNS complication. It is said to be characteristic in the order
microorganisms and to determine their toxigenicity.
administered as a single empirical dose of 20,000-120.000 U based on the degree of toxicity. site and size of the membrane, and duration of
Pathogenesis: The degree of local extension correlates directly with profound prostration, bull-neck appearance, and fatality due to airway and time of appearance. Also it is said to be completely reversible, if patient
survives. Paralysis may occur as follows: Palatal: usually is seen around the third 🔹
illness. Antitoxin is not recommended for asymptomatic carriers.
Antibiotic: C. diphtheriae is usually susceptible to various agents in vitro, including penicillins, erythromycin, clindamycin, rifampin, and
The organism usually remains in the superficial layers of skin lesions or respiratory tract mucosa, inducing local inflammatory reaction. The
🔹
compromise or toxin-mediated complications.
week of illness and it may be uni or bilateral. Is the commonest form. Ocular: Seen by
🔹
Differential diagnosis: tetracycline. Erythromycin is marginally superior to penicillin for eradication of nasopharyngeal carriage. Appropriate therapy is erythromycin
🔹
Laryngeal: Rarely it is a primary site of diphtheria. Usually is secondary to a pharyngeal infection. It is a serious form that Nasal: Foreign bodies, acute rhinitis etc.
major virulence of the organism lies in its ability to produce the exotoxin, which inhibits protein synthesis and causes local tissue necrosis. progresses in three phases: an early dysphonic phase (hoarseness, stridor and barking cough) for around 24 hours followed by the third week or 1-2 weeks later. The commonest ocular paralysis reported is that
Tonsillar and or pharyngeal: Exudative pharyngitis caused by Streptococcus
(40-50 mg/kg/24 hr divided q 6 hr PO or IV; aqueous crystalline penicillin G (100,000-150,000 U/kg/24 hr divided q 5 h IV or IM), or procaine
Within the first few days of respiratory tract infection (usually in the pharynx), a dense necrotic coagulum of organisms, epithelial cells,
fibrin, leukocytes, and erythrocytes forms, advances, and becomes a gray-brown, leather-like adherent pseudomembrane. Removal is difficult
the dyspneic phase with increased dyspnea and severe progressive retractions for about 48 hrs, then the asphyctic stage
which is terminal characterized by cyanosis, restlessness and death.
of the accommodation (blurred vision). Secondly is the extrinsic muscles paralysis.
May last for around 1 week. Facial: Occurs by the 3rd 5th week. May be uni or
bilateral. Pharyngeal, laryngeal, respiratory, cardiac, and limbs paralysis may occur 🔹
pyogenes or Epstein-Barrvirus. Vincent angina, infectious mononucleosis, etc.
Laryngeal: bacterial epiglottitis, severe viral laryngotracheobronchitis, etc
🔹
penicillin (25,000-50,000 U/kg/24 hr divided q 12 h IM). Therapy is given for 14 days.

🔹 Some patients with cutaneous diphtheria have been treated for 7-10 days.
Elimination of the organism should be documented by at least 2 successive negative cultures from the nose and throat (or skin) obtained 24
and reveals a bleeding edematous submucosa. Paralysis of the palate and hypopharynx is an early local effect of diphtheritic toxin. Cutaneous diphtheria: Classic cutaneous diphtheria is an indolent, non progressive infection characterized by a superficial, between the7thand 10th weeks. hr apart after completion of therapy.
Toxin absorption can lead to systemic manifestations: kidney tubule necrosis, thrombocytopenia, cardiomyopathy, and demyelination of ecthymic, nonhealing ulcer with a gray-brown membrane.Diphtheria at other sites: (iii) Renal: Renal tubular necrosis. Oliguria and proteinuria indicate kidney
complications
nerves. Because the latter two complications can occur 2-10 wk after mucocutaneous infection, the pathophysiologic mechanism in some • The ear (otitis external), the eye (purulent and ulcerative conjunctivitis), and the genital tract (purulent and ulcerative
vulvovaginitis).
cases is suspected to be immunologically mediated.



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