State University of Medicine and Pharmacy “Nicolae

Testemitanu”
 Department of Infectious diseases

Angina (streptococcal diphtheria, herpes,

mononucleosis). Mumps.

Cojuhari Lilia
Associate professor
• Tonsils are large
lymphoid tissue situated
in the lateral wall of the
oropharynx.
• They form lateral part
of the Waldeyer's ring.
• Tonsil occupies the
tonsillar fossa between
diverging palato-
pharyngeal and
palatoglossal folds
• Tonsil has two surfaces, medial and lateral;
two borders anterior and posterior; two poles
upper and lower; two developmental folds
plica triangularis and plica semilunaris; and
one cleft intratonsillar cleft.
• Medial surface is covered by squamous
epithelium and presents 15-20 crypts usually
plugged with epithelial and bacterial debris
• Lateral surface extends deep to surrounding
boundaries. It is coated with a fibrous sheet,
an extension of pharyngobasilar fascia called
capsule of the tonsil.
• The capsule is loosely attached to the
muscular wall but antero-inferiorly it is
attached firmly to the side of the tongue just
in front of insertion of palatoglossus and
palatopharyngeus muscles
Acute tonsillitis

Acute tonsillitis are

inflammation which
include lymphatic
Waldeyer ring, posterior
pharynx, oropharynx,
lueta, tonsillar pillars,
soft palate caused by
bacterial, viral or
fungal.
 Etiology

• A common cause is Streptococcus (strep) bacteria.

Other common causes include:
• Adenoviruses
• Influenza virus
• Epstein-Barr virus
• Parainfluenza viruses
• Enteroviruses
• Herpes simplex virus
 Classification (1)
After etiology
• infectious tonsillitis (angina)
• viral
• bacterial
• fungal
• Tonsillitis noninfectious
• Immuno-allergic
• Physico-chemical (burns, nicotine)
After evolution
• acute
• chronic
 Classification (2)
1. Acute catarrhal or superficial tonsillitis. Here tonsillitis
is a part of generalised pharyngitis and is mostly seen
in viral infections.
2. Acute follicular tonsillitis. Infection spreads into the
crypts which become filled with purulent material,
presenting at the openings of crypts as yellowish
spots.
3. Acute parenchymatous tonsillitis. Here tonsil substance
is affected. Tonsil is uniformly enlarged and red.
4. Acute membranous tonsillitis. It is a stage ahead of
acute follicular tonsillitis when exudation from the
crypts coalesces to form a membrane on the surface
of tonsil.
 Catarrhal tonsillitis

When tonsils are

inflamed as part of
the generalised
infection of the
oropharyngeal
mucosa it is called
catarrhal tonsillitis.
 Membranous tonsillitis

Some times exudation

from crypts may
coalesce to form a
membrane over the
surface of tonsil,
giving rise to clinical
picture of membranous
tonsillitis.
 Parenchymatous tonsillitis

When the whole tonsil

is uniformly
congested and swollen
it is called acute
parenchymatous
tonsillitis
 Clinical manifestations
The main symptoms of tonsillitis are inflammation and swelling of the tonsils, sometimes severe enough
to block the airways.
• Other symptoms include:
Throat pain or tenderness
Redness of the tonsils
A white or yellow coating on the tonsils
Painful blisters or ulcers on the throat
Hoarseness or loss of voice
Headache
Loss of appetite
Ear pain
Difficulty swallowing or breathing through the mouth
Swollen glands in the neck or jaw area
Fever, chills
Bad breath
• In children, symptoms may also include:
Nausea
Vomiting
Abdominal pain
 Diagnosis
• The diagnosis of tonsillitis can be confirmed by culture
of samples obtained by swabbing both tonsillar surfaces
and the posterior pharyngeal wall and plating them on
sheep blood agar medium. The isolation rate can be
increased by incubating the cultures under anaerobic
 conditions and using selective growth media.
• A single throat culture has a sensitivity of 90%-95%.
• Newer tests identify GABHS serotypes using nucleic
acid (DNA) probes or polymerase chain reaction. 
• Bacterial culture may need to be performed in cases of a
negative rapid streptococcal test.
 Treatment (1)
• Treatments to reduce the discomfort from tonsillitis symptoms
include:
• pain relief, anti-inflammatory, fever reducing medications (
paracetamol/acetaminophen and/or ibuprofen)
• sore throat relief (warm salt water gargle, lozenges, dissolved aspirin
gargle (aspirin is an anti inflammatory, do not take any other anti
inflammatory drugs with this method), and iced/cold liquids)
• If the tonsillitis is caused by group A streptococcus, then antibiotics
 are useful with penicillin or amoxicillin being primary
choices. Cephalosporins and macrolides are considered good
alternatives to penicillin in the acute setting. A macrolide such as 
erythromycin is used for people allergic to penicillin. Individuals
who fail penicillin therapy may respond to treatment effective
against beta-lactamase producing bacteria  such as clindamycin or 
amoxicillin-clavulanate.
 Treatment (2)
• If the tonsillitis is caused by a virus, antibiotics won't work
and your body will fight off the infection on its own. In the
meantime, there are things you can do to feel better,
regardless of the cause. They include:
• Get enough rest
• Drink warm to ease throat pain
• Eat smooth foods, such as flavored gelatins, or applesauce
• Use a cool-mist vaporizer or humidifier in your room
• Gargle with warm salt water
• Suck on lozenges containing benzocaine or other anesthetics
• Take over-the-counter pain relievers such as acetaminophen
 or ibuprofen.
 Acute herpetic gingivostomatitis
● Usually infects children from 6 months to 3 years old.
● The disease frequently occurs in primary infection.
● The disease has an acute onset with severe toxemic
fever (up to 40-41°C). Child stops eating, complains
of sore mouth, severe hypersalivation. At the same
time hyperemia and edema of mucous membranes of
cheeks, gums, tongue, and lips appear.
● Soon after typical herpetic eruptions occur in their
place; they burst rapidly, resulting in aphthae.
● Regional lymph nodes are enlarged and painful.
● Duration of the disease is from 7 to 10 days.
 Diphtheria is an acute infectious disease caused by
Corynebacterium diphtheria and characterized by the
appearance of a fibrinous membrane on the site of pathogen
invasion, which can spread on to the tonsils, larynx and
pharynx, leading to symptoms of toxemia and toxic lesions
of the cardiovascular system, nervous system, adrenal
glands and kidneys.
Clinical manifestations of oropharyngeal
diphtheria
Duration of the incubate period is from 2 till 10
days.
 The localized form of oropharyngeal
diphtheria (1)
 mild or moderate toxemia
 local inflammation process, encompassing the area of
tonsils.
 indisposition,
 anorexia,
 subfebrile body temperature,
 the throat is moderately sore,
 regional lymph nodes are moderately enlarged and
painful.
 Classification of clinical forms of diphtheria

• Frequent clinical forms:

1. Diphtheria of nasopharynx and tonsil;
2. Diphtheria of larynx and trachea;
3. Diphtheria of front department of nose.
 The localized form of oropharyngeal
diphtheria (2)
Forms:
1. Localized (catarrhal, insular, membranous);
2. Spread form;
3. Toxic form:
- I degree,
- II degree,
- III degree,
4. Hypertoxic;
5. Hemorrhagic form;
6. Gangrenous form;
7. Associated (pharynx+eyes+nose+larynx, and others).
• Rare forms of Diphtheria (which nowadays are no longer
met):
1. Diphtheria of eyes;
2. Diphtheria of skin;
3. Diphtheria of mouth;
4. Diphtheria of reproductive organs;
5. Diphtheria of wounds.
 The catarrhal (atypical) form
 Is registered in the foci of diphtheria.
 Moderate congestive hyperemia of oropharyngeal
mucous membrane.
 Symptoms of intoxication are absent or moderate.
 The body temperature is normal or subfebrile.
 Reaction of the regional lymph nodes is not
expressive.
 The diagnosis is confirmed by test results which
show C.diphtheriae.
 In the vaccinated children.
 It is caracterized by typical fibrinous membranes in the form
of grayish-white points, strips; small islands located out of
the lacunae. The patches may be taken off without difficulty
and bleeding of the mucous membrane may act be present.
 The body temperature increases to subfebrile.
 Expressed symptoms of intoxication are absent. The throat
has no severe symptoms.
 Congestive hyperemia and moderate edema of
oropharyngeal mucous membrane are found.
 Regional lymph nodes are moderately enlarged and painful.
 Timely bacteriologic tests have great significance in the
diagnosis of diphtheritic infection.
 The complications are rare in this form of tie disease. There
can be mild forms of myocarditis.
Pharyngeal diphtheria with membranes
covering the tonsils and uvula.
 The widespread form of oropharyngeal diphtheria

 Is characterized by spreading of fibrinous membranes

beyond the borders of the tonsils, on to the soft palate,
lateral and back walls of the oropharynx, the palatal
arches, the uvula.
 The mucous membrane of oropharynx is edematous.
 Regional lymph nodes are enlarged and painful.
 The body temperature increases up to 39°C, and
higher.
 Headache, weakness, sore throat, are present.
 Clinical manifestation of cardiovascular disorders are
present since the onset.
 The toxic (severe) form (1)
• The onset is acute.
• The body temperature is 40 °C or higher.
• Severe headache, vomiting, anorexia, pallor,
increasing weakness
• The mucous membranes are edematous, with a
cyanotic hue.
• The tonsils are enlarged, their surface is covered
with thick whitish-grey, dirty-grey, or grey
membranes with a rough surface. The membranes
may be thin and taken off easily at the first hours
of the disease. But they appear on the site again.
 The toxic (severe) form (2)
 The membranes spread to uvula, soft and hard palate,
the back wall of the pharynx.
 There is severe edema of the mucous membrane of the
oropharynx and adipose tissue of the neck.
 Depending on the spreading of edema three forms of
toxic diphtheria:
 the toxic form of the 1st degree - to the middle of the
neck,
 the toxic form of the II-rd degree - to the clavicles,
 the toxic form of the III-rd degree - below the
clavicles.
Bull neck appearance of diphtheritic
cervical lymphadenopathy
 Hypertoxic form
Characterized by an abrupt onset and rapid development.
Increasing toxemia is manifested by fever, severe prostration,
mental confusion, convulsions since the first hours of the
disease.
The course is culminant.
Symptoms of intoxication predominate in the clinical
manifestations of the disease and they leave behind the
appearance of the membranes, edema of mucous membranes of
oropharynx and adipose tissue of the neck.
 ITS is manifested by striking pallor, acrocyanosis, a drop of
temperature of the skin and its “marmoreal” look, rapid thready
pulse, dull heart sounds, decrease of blood pressure, oliguria.
Lethal outcome will usually come on the 2nd-3rd day after the
onset from progressive cardiovascular failure.
Nasal diphtheria
 Antitoxic therapy

• Antitoxic therapy must be given promptly and

in adequate dosage. Any delay increases the
possibility that myocarditis, neuritis or death
may occur
 Antibacterial therapy
 Penicillin, ampicillin, erythromycin, cephalosporin are effective
medications against most strains of C.diphtheria.
 In severe forms of the disease antibiotics should be given
parenterally: penicillin, ampicillin, cephalosporins in a daily
dosage of 50-100 mg/kg.
 The treatment course must last till the liquidation of local process,
but its duration must not be over 10-14 days.
 Antibacterial therapy is not a substitute for antitoxin treatment.
Eradication of the organism should be documented by culture.
 Persons who continue to harbour the organism after treatment,
should take a recurrent course of therapy of another antibiotic
during 7 days and follow-up cultures should be obtained.
 Diphtheria carriers should be treated using a similar scheme
 Prophylaxis

• DTP priming vaccine age 2, 4 and 6 months,

revaccination with DTP 22-24 months Td
other revaccination 6-7 years and 14-15 years,
then every five years up to 40 and every 10
years to 60 years.
 Mumps (Epidemic Parotitis)

Mumps is an acute, systemic, communicable viral

infection whose most distinctive feature is swelling of
one or both parotid glands.
Involvement of other salivary glands, the meninges,
the pancreas, and the gonads is also common.
 ETIOLOGY

● The causative agent in mumps is a filterable virus

from the group of Paramyxovirus parotiditis
● It contains ribonucleic acid (RNA).
 Epidemiology
● The source of infection is a patient. Patients with an
atypical forms of mumps are of epidemiological value.
● Infection is transmitted:
 mainly by the aerial-droplet route,
 by various objects contaminated by the patient's
saliva (such as dishes, toys, etc.) if they are passed to a
healthy child within a short time and he puts them into
his mouth.
• The disease shows a seasonal prevalence, with the
greatest incidence in winter and spring.
 Clinical Manifestations (1)
● The incubation period of mumps
lasts on average for 18 to 20 days,
but extremes of 11 and 23 days
occur.
● Its onset is characterized by
elevation of temperature (up to
38°C or 39°C)
● Swelling of the parotid gland
(usually on one side, but sometimes
on both). The swelling obliterates
the fossa retromaxillaris and may
spread downwards anteriorly and
posteriorly to the neck.
 Clinical Manifestations (2)
• The centre of the swelling is elastic-solid on palpation and
painful when pressed. At times the painless spreads to the face
and far to the neck.
● The skin over the inflamed gland is tense and lustrous, but
remains usually of normal color.
● Swelling of the parotid gland is accompanied with pain
irradiating to the ear or neck, that becomes more intense
during chewing or swallowing.
● In one or two days the parotid gland on the opposite side may
become involved; and in about half the cases the
submandibullary, and sometimes the sublingual, glands are
affected.
● Submandibullitis is sometimes accompanied with extensive
edema of the cervical cellular tissue.
 Clinical Manifestations (3)

● The swelling of the affected gland increases for the

first three to five days, then begins to regress and
subsides by the eighth to tenth day.
● Simultaneously with subsidence of inflammation the
temperature falls, the pain declines, and the patient's
general condition improves.
● If several glands are affected one after the other the
disease may last for two and more weeks.
● The orifice of Stenon’s duct is commonly red and
swollen.
This is a photograph of a patient with bilateral swelling
in his submaxillary regions due to mumps.
 Degree of a swelling of salivary glands

I degree – a swelling of salivary glands is

defined only at a palpation;
II degree – a swelling of salivary glands is
defined not only at palpation, but also visually
III degree – a swelling of salivary glands is
expressed and accompanied by a hypostasis of
a hypodermic cellulose of a neck.
This is a photograph of a patient with bilateral swelling
in his submaxillary regions due to mumps
 Diagnosis and Prognosis

 Difficulties in diagnosing mumps occur in mild and

abortive forms, and when only submandibullary
glands are affected, or the meningitis or orchitis is
manifestation.
 Diagnosis is established from the features of the
clinical course described above and the
epidemiological data.
 TREATMENT
● Treatment is symptomatic.
● Diet is restricted to fluids or semifluids to spare the affected glands. Heat is
applied to the glands by means of cotton or wool bandages, Sollux lamp,
etc.
● The administration of analgesics and the application of warm compresses
to the parotid area may be helpful.
● The mouth should be rinsed with weak disinfecting solutions.
● Strict confinement to bed is called for in orchitis; the testis should be
supported and cold applied.
● Testicular pain may be minimized by the local application of cold
compresses and gentle support for the scrotum.
● Corticosteroid preparations produce considerable alleviation of pain and
subjective improvement.
● To relieve the severe headache and other meningeal symptoms in
concomitant meningitis lumbar puncture.
● Dehydration therapy is carried out.
 TREATMENT
● Corticosteroids:
 Prednisolon 1-2 mg/kg/24 de ore i.m. – 5-10 zile
or
 Dexametazonă 0,1-0,2 mg/kg/24 ore – 5-10 zile.
● Non-steroidal anti-inflammatory drugs::
 Ibuprofen: 1-12 ani – 30-40 mg/kg pe zi divizată în
3-4 prize pentru perioada acută a bolii
● Antibiotics:
 Ampicilină – 500 mg de 4 ori pe zi, i.m., 7 zile, sau
 Amoxicilină – 500 mg de 3 ori pe zi, per os, 7 zile
Discharge from the hospital - 5-6 days after the
disappearance of local signs.
 PREVENTION (1)
● The patient is isolated at home. Hospitalization is
indicated only in individual cases when the course of
the disease is severe or there are epidemic indications.
Considering that the patients are infective for a
relatively short time the period of isolation has been
reduced to 9 days.
● Contacts who have not previously had the disease
should be segregated on the 21st day from the
beginning of the disease. When the time of their contact
is definitely known, they are allowed to attend the
children's institution during the first ten days of
incubation, and are only isolated from the 11-th to the
21-st day from the time of contact.
 PREVENTION (2)
● The subcutaneously administered vaccine may be
given to children older than 1 year but is not
recommended for younger infants because of the
potential for interference by passive maternal
antibodies.
● Mumps vaccine is usually administered as part of the
measles-mumps-rubella (MMR) vaccine at the age of
12 to 15 months and again at 6 to 7 years of age. This
MMR vaccine is also recommended for susceptible
older children adolescents, and adults, particularly
adolescent males who have not had mumps.
 Infectious Mononucleosis
• Infectious mononucleosis is a contagious disease.
• It is common among teenagers and young adults, especially
college students.
• At least one out of four teenagers and young adults who get
infected with EBV will develop infectious mononucleosis.
 Transmission

• bodily fluids, especially saliva.

• However, these viruses can also spread through blood and
semen during sexual contact, blood transfusions, and organ
transplantations.
 Diagnosis

• by symptoms 
• EBV infection can be confirmed with a blood test that detects
antibodies. About nine out of ten of adults have antibodies that
show that they have a current or past EBV infection.
• For more information, are Laboratory Testing.
DIAGNOSIS
 Laboratory Testing (1)

• Viral capsid antigen (VCA)

• Anti-VCA IgM appears early in EBV infection and usually
disappears within four to six weeks.
• Anti-VCA IgG appears in the acute phase of EBV infection,
peaks at two to four weeks after onset, declines slightly then
persists for the rest of a person’s life.
• Early antigen (EA)
Anti-EA IgG appears in the acute phase of illness and
generally falls to undetectable levels after three to six months.
In many people, detection of antibody to EA is a sign of active
infection. However, 20% of healthy people may have
antibodies against EA for years.
 Laboratory Testing (2)
• EBV nuclear antigen (EBNA)
Antibody to EBNA, determined by the standard
immunofluorescent test, is not seen in the acute phase of EBV
infection but slowly appears two to four months after onset of
symptoms and persists for the rest of a person’s life. Other
EBNA enzyme immunoassays may report false positive
results.
 Interpretation of EBV antibody tests and
diagnosis of EBV infection 
• Susceptibility to infection
People are considered susceptible to EBV infection if they do
not have antibodies to the VCA.
• Primary (new or recent) infection
People are considered to have a primary EBV infection if they
have anti-VCA IgM but do not have antibody to EBNA. Other
results that strongly suggest a primary infection are a high or
rising level of anti-VCA IgG and no antibody to EBNA after at
least four weeks of illness. Resolution of the illness may occur
before the diagnostic antibody levels appear. In rare cases,
people with active EBV infections may not have detectable
EBV-specific antibodies.
 Interpretation of EBV antibody tests and
diagnosis of EBV infection
• Past infection
The presence of antibodies to both VCA and EBNA suggests
past infection (from several months to years earlier). Since
over 90% of adults have been infected with EBV, most adults
will show antibodies to EBV from infection years earlier. High
or elevated antibody levels may be present for years and are
not diagnostic of recent infection.