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PHARYNGITIS
Acute pharyngitis is an inflammatory syndrome of the pharynx caused by several different
groups of micro-organisms. Most cases are of viral etiology and occur as part of common
colds and influenzal syndromes. The most important of the bacterial infections is that
caused by Group A  haemolytic Streptococci (Strep. Pyogenes). It is important to
differentiate streptococcal from viral pharyngitis because of the response of streptococcal
infection to penicillin therapy and the ineffectiveness of antibiotic therapy in the viral
infections. Also, streptococcal pharyngitis may be complicated by acute rheumatic fever and
acute glomerulonephritis.
ETIOLOGY
Microbial Causes of Acute Pharyngitis
Pathogen
Viral
Rhinovirus (100 types and 1 subtype)
Coronavirus (3 or more types)
Adenovirus (types 3, 4, 7, 14, 21)
Herpes simplex virus (types 1 and 2)
Parainfluenza virus (types 1-4)
Influenza virus (types A and B)
Cocksackievirus A (types 2, 4-6, 8, 10)
Epstein-Barr virus
Cytomegalovirus
HIV-1
Bacterial
Streptococcus pyogenes (group A
-hemolytic streptococci)
Group C -hemolytic streptococci
Mixed anaerobic infection
Neisseria gonorrhoeae
Corynebacterium diphtheriae
Corynebacterium ulcerans
Arcanobacterium haemolyticum
(Corynebacterium haemolyticum)
Yersinia enterocolitica
Treponema pallidum
Chlamydial
Chlamydia pneumoniae
Mycoplasmal
Mycoplasma pneumoniae
Mycoplasma hominis (type 1)
Unknown
Syndrome/Disease
Common cold
Common cold
Phayrngoconjunctival fever, ARD
Gingivitis, stomatitis, pharyngitis
Common cold, croup
Influenza
Herpangina
Infectious mononucleosis
Infectious mononucleosis
Primary HIV infection
Estimated
Importance
20
5
5
4
2
2
<1
<1
<1
<1
Pharyngitis/tonsillitis, scarlet fever
15-30
Pharyngitis/tonsillitis
Gingivitis, pharyngitis
(Vincent’s angina)
Peritonsillitis/peritonsillar abscess
(quinsy)
Pharyngitis
Diphtheria
Pharyngitis, diphtheria
Pharyngitis, scarlatiniform rash
5-10
<1
Pharyngitis, enterocolitis
Secondary syphilis
<1
<1
1
<1
<1
<1
<1
Pneumonia/bronchitis/pharyngitis
Unknown
Pneumonia/bronchitis/pharyngitis
Pharyngitis in volunteers
<1
Unknown
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Approximately 15% of all cases of pharyngitis are due to S. pyogenes. Strep. of Group C
and B have also been implicated in some cases.
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EPIDEMIOLOGY
Most cases of pharyngitis occur during the colder months of the year, during the respiratory
disease season.
PATHOGENESIS
Symptoms of sore or scratchy throat occur in approximately 50% of people with rhinovirus
colds and in 20-70% of people with respiratory illness due to coronavirus. The pathogenetic
mechanisms are different for the various organisms.
The events leading to invasive Strep. infection of the pharynx and tonsil are also not well
understood. Pharyngeal carriage of S. pyogenes is commonly observed in asymptomatic
people. Factors that influence the balance between colonisation and invasive infection may
include natural and acquired host immunity and interference among the bacteria present in
the oropharynx. S. pyogenes elaborates a number of extracellular factors, including
erythrogenic toxins, haemolysins, streptokinase etc. which are of known or possible
pathogenic importance. Complications of acute streptococcal pharyngitis may include:
1.
2.
3.
Acute rheumatic fever.
Acute glomerulonephritis
Invasive infection
There is a general association of specific M serotypes with these complications. It is likely,
however, that strain related virulence factors rather than M serotype per se are the major
determinant of disease expression.
The usual pathologic changes occurring in viral pharyngitis are oedema and hyperaemia of
the tonsils and the pharyngeal mucous membranes. An inflammatory exudate may be
present with adenovirus and EBV infections. Vesiculation and mucosal ulceration may occur
with HSV and some cocksackievirus A infections. With Strep. tonsillopharyngitis, there is an
intense inflammatory response characterised by marked erythema and oedema of the uvula
and frequently the presence of a greyish-yellow tonsillar exudates. With diphtheria a fibrous
pseudomembrane containing necrotic epithelium, leukocytes and bacterial colonies develops
on the epithelial surface.
CLINICAL PRESENTATION
Streptococcal pharyngitis: Severity of illness associated with S. pyogenes infection of the
pharynx varies greatly. In severe cases, there is marked pharyngeal pain, difficulty in
swallowing and a pyrexia of 39C or greater.
Headaches, chills and abdominal pain may occur. The pharyngeal membrane is a fiery red,
and a patchy, grey-yellow exudates is present on the tonsils. There is often marked uvular
oedema. Tender, enlarged cervical nodes and a leukocyte count of over 12,000/ mm3 are
invariably present. At the other extreme are those Strep. infections that are quite mild or
may often go unrecognised by the patient. Infection with strains of S. pyogenes that produce
erythrogenic toxin results in the characteristic erythematous rash of scarlet fever, which is
followed by desquamation. It has recently been reported that non-invasive pharyngitis due
to S. pyogenes may be the cause of streptococcal toxic shock syndrome. The clinical
features of pharyngitis with strains of Group C and G streptococci are similar to those of
S. pyogenes.
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Anaerobic Pharyngitis (Vincent’s angina): Pharyngeal and tonsillar infection with a
mixture of anaerobic bacteria and spirochatese still occurs but is uncommon. In this
infection a purulent exudates coats the membrane and there may be a foul odour on the
breath. The disease is most common in adolescents and young adults.
Peritonsillar Abscess (Quinsy): May be due to a mixture of organisms. Pharyngeal pain
is usually severe and dysphagia and low-grade fever are common. The infection is usually
limited to one side.
Gonococcal Pharyngitis: Incidence has increased in recent years. Most infections are
asymptomatic but gonorrhoeal infection may be responsible for an occasional case of mild
pharyngitis.
Infectious Mononucleosis: Exudative tonsillitis or pharyngitis occurs in approximately one
half of the cases of infectious mononucleosis due to EBV. Fever and cervical adenopathy
are characteristically present. May also have other features of the disease such as
headache and persistent malaise and fatigue. Generalised lymphadenopathy may be
present and there is splenomegaly is approximately half the cases. The mononucleosis
syndrome is also associated with CMV infection.
Diphtheria: Uncommon today. Disease characteristically has a slow onset and pharyngeal
discomfort is usually not marked. Low grade pyrexia is present. The characteristic tonsillar
or pharyngeal membrane varies in colour from light to dark grey and is firmly adherent to the
tonsil and pharyngeal mucosa.
Chlamydial Pharyngitis: C. pneumoniae (strain TWAR) has been established as an
aetiologic agent of acute infections of the respiratory tract – some of which have pharyngeal
manifestations.
Mycoplasmal Pharyngitis: Epidemiologic studies of pharyngitis have associated some
cases with M. pneumoniae infection. The illness observed has been relatively mild and have
no distinguishing clinical features.
Diagnosis: The primary objectives in the diagnosis of acute pharyngitis are to distinguish
cases of common viral etiology from those due to S. pyogenes and to detect and identify the
occasional case due to an unusual or rare cause for which treatment is available. In the
majority of cases, an etiologic diagnosis is not possible on clinical grounds alone. Take
throat swabs for culture and sensitivity testing when examining the pharyngeal area. There
are also various tests for some suspected viral causes, e.g. EBV.
TREATMENT & PREVENTION
Streptococcal pharyngitis – Antimicrobial therapy: Patients should receive a 10 day
course of penicillin or an equivalent antibiotic if they are allergic to penicillin, e.g.
Erythromycin. Recurrences may occur. You need to treat to prevent the development of
rheumatic fever, to limit transmission to school and household contacts and for prevention of
suppurative complications of Strep. pharyngitis which are sinusitis, otitis media, mastoiditis,
and also including bacteraemia and pneumonia.
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Sinusitis: Is an inflammation of the mucosal lining of the paranasal sinuses and is a
common disorder in both children and adults.
Microbial causes of acute sinusitis:
Bacteria
- Strep. pneumoniae
H. influenzae
Anaerobes
Staph. Aureus
Strep. pyogenes
Branhamella catarrhalis
Viruses
-
Rhinoviruses
Influenza
Parainfluenza
Clinical presentation: Headaches, pain and facial swelling. Sometimes cough and nasal
discharge.
Diagnosis: X-Ray and sinus aspiration. Specimens to the laboratory for analysis.
Treatment: Amoxycillin/Clavulanate for 10 days. Alt. Erythromycin ± drainage.
Otitis media: Common in children. Presenting features – fever, irritability, ear pain. On
examination the tympanic membrane is full or bulging. There may be a purulent discharge if
a perforation is present.
Diagnosis: Culture of pus for the ear or perhaps diagnostic aspiration.
Bacteria involved:
- Strep. pneumoniae
H. influenzae
B. catarrhalis
Management: Most experts agree that patients who have the signs and symptoms of acute
Otitis media should receive antimicrobial therapy – however several reports recently have
questioned this. Recommend antibiotics – Ampicillin/Amoxycillin – Erythromycin if allergic to
penicillin. Consider the use of Amoxycillin/Clavulanate if resistant strains are isolated.
Myringotomy with tympanostomy may be necessary in patients with recurrent episodes of
Otitis media.
Acute epiglottis (Supraglottitis): First described in 1900. Is characterised by a severe
URTI with fever, sore throat, hoarseness, dysphagia and drooling that may rapidly progress
to fatal airway obstructioin. Most commonly affects children 2-7 years of age but is
(obviously) undergoing a dramatic and changing epidemiology pattern since the introduction
of Hib vaccines in the late 1980s. Epiglottitis may become a disease of older children and
adults and may be due to microbial pathogens other than H. influenzae Type b.
Microbiology: Bacterium involved in most cases in children is H. influenzae Type b
(capsulate) other pathogens have included:
S. pneumoniae
S. aureus
H. parainfluenzae
The isolation rate for H. influenzae from blood cultures is 80-100%. Epiglottitis is
responsible for 1 of 1000-2000 admissions to a children’s hospital. It is characterised by
inflammation and oedema of the supraglottic structure including the epiglottis. It may arise
from direct invasion by H. influenzae or other pathogens.
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Clinical Manifestations: For children – severe sore throat, high fever, drooling and airway
obstruction which, left untreated, may lead to death. On examination the child looks toxic
and apprehensive and may be sitting upright. Presentation may be more variable in adults.
Diagnosis: Definitive diagnosis is made by examination of the epiglottis and supraglottic
structures – however, no attempt should be made to visualise the epiglottis in an awake
young child – one may cause spasm and lead to complete airways obstruction. The
epiglottis is usually red and swollen. Laboratory findings include raised white cell count and
positive blood cultures. X-Ray may show a characteristic picture.
Treatment: Directed at established of an airway and administration of antibiotics.
Amoxycillin/Clavulanate is the recommend antimicrobial.
Prevention: Rifampicin prophylaxis recommended for:
1.
2.
3.
All household contacts when there are susceptible members
<4 years of age;
Daycare and nursery school classroom contacts and
The patient who should receive Rifampicin before discharge.
Vaccination with the Hib vaccine has proved to be very effective.
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PNEUMONIA
a)
Community Acquired
b)
Hospital Acquired (nosocomial)
MICROBIOLOGY OF COMMUNITY-ACQUIRED PNEUMONIA
Microbial Agents:
Bacteria
-
Strep pneumoniae
H. influenzae
B. catarrhalis
S. aureus
Gram negative bacilli, e.g. Klebsiella
Strep. pyogenes
Atypical
-
Legionella spp.
Mycoplasma pneumoniae
Chlamydia pneumoniae
Viral
NOSOCOMIAL PNEUMONIA
Risks for nosocomial pneumonia may be considered –
1.
2.
3.
Rate
Patient related.
Infection Control related.
Intervention related.
0.5-1%
15-20%
18-60%
of all hospitalised persons;
is the reported rate for intensive care units;
for mechanically ventilated patients.
Bacteriology: Studies indicate that Gram Negatives account for 50-70% of cases.
BACTERIAL PNEUMONIA
Pneumococcal – frequency: Estimated annual rate of pneumococcal pneumonia is 1 to 10
per 1000 in the U.S., with an annual total of about 500,000.
Microbiology: S. pneumoniae is a Gram Positive coccus which usually appears in pairs. It
is  haemolytic. It is identified by its susceptibility to Optochin. Pathogenicity is related to
the polysaccharide capsule with at least 84 identified serotypes. The major use of
serotyping is for epidemiologic investigation and for implementing strategies for disease
control with pneumococcal vaccine, which contains polysaccharides of the 23 serotypes that
account for 89% of invasive infections caused by S. pneumoniae.
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Pathogenesis:
The usual mechanism of pneumonia is by aspiration of
S. pneumoniae that is harboured in the nasopharynx. Colonisation rates are highly variable
but usually reported at 5% to 30% among healthy adults.
Risk factors:
Age
Chronic pulmonary disease
Congestive cardiac failure
Cigarette smoking
HIV Infection
Post splenectomy
Clinical Features: The classic presentation is a dramatic illness characterised by abrupt
onset with a rigor followed by high fever, cough with production of purulent sputum,
dyspnoea and pleuritic pain. In the absence of treatment this might last for 7 to 10 days.
Laboratory studies usually show leucocytosis with a left shift, hypoxaemia and changes on
chest X-Ray. The classic X-Ray finding is that of a lobar pneumonia.
Diagnosis: An established diagnosis requires recovery of S. pneumoniae from an
uncontaminated specimen source including blood, pleural fluid or sputum. Need to Gram
stain and culture sputum.
Treatment: Penicillin has been the drug of choice but with the advent of strains resistant to
penicillin (and other antibiotics) one has to consider other options. The degree of resistance
varies between intermediate and high level (MIC >2 mg/L). In this hospital, all of our
resistant isolates have been of the intermediate type.
Complications and response to therapy: Major complications of patients hospitalised with
pneumococcal pneumonia arise in the following % of cases:
12%
0.5 -1%
0.3 - 0.5%
Bacteraemia
Empyaema
Meningitis
Overall mortality rate in hospitalised patients in the U.S. is 12%
Prevention:
Polyvalent pneumococcal vaccine that includes 23 serotypes of
S. pneumoniae that account for about 89% of pneumococcal disease. The vaccine is
recommended for:
1.
2.
3.
4.
5.
6.
7.
Persons over 65 years
HIV infection
Chronic renal failure
Alcoholism
Asplenia
Diabetes mellitus
Chronic obstructive lung disease.
Re-vaccination is recommended after 5 years in those at high risk.
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Staph. aureus pneumonia: Rare in adults without specifically defined defects as follows:
1.
Nosocomial pneumonia – 2nd only to GNBs in frequency. Is especially common
in ventilator associated pneumonia.
2.
Postinfluenza pneumonia – 2nd only to S. pneumoniae in frequency.
3.
Septic pulmonary embolism especially with tricuspid valve endocarditis
associated with I.V. drug abuse.
4.
Structural disease of the lung including Cystic Fibrosis and Bronchiectasis.
Gram-negative pneumonia: Largely a product of the antibiotic era.
1.
Mainly Enterobacteria and Pseudomonas spp. These are rare causes of
Community Acquired Pneumonia.
2.
These are major causes of nosocomial pneumonia accounting for 30-60% of
cases in most series.
4.
Pneumonia usually follows aspiration of these organisms when they reside in the
upper airways or stomach. Treatment consists of supportive measures and
antibiotics directed against the implicated pathogens.
ATYPICAL PNEUMONIA
Mycoplasma pneumoniae: Does not have a cell wall. Accounts for 2-15% of community
acquired pneumonias. Incidence is age dependent – more common in adolescents and
young adults. The pneumonia is usually self-limited and develops in only 5- 15% of exposed
persons. A dry hacking cough, low grade fever and headache are characteristic. Bibasal
interstitial infiltrates may be seen on X-Ray. Isolation of mycoplasma is difficult. Cold
agglutination antibody may be positive in up to 70% of cases. Diagnosis is often made on
serologic studies, i.e. to demonstrate a fourfold rise in serum antibody levels (acute and
convalescent sera required).
Treatment: Erythromycin or Tetracycline.
LEGIONELLA: Species of Legionella, primarily L. pneumophila, serogroup 1, account for 26% of community-acquired pneumonias. May affect persons of all ages but the incidence is
slightly higher in elderly or debilitated persons. Legionella spp. are far more virulent than
other atypical pathogens. Mortality rates of 10-20% have been reported. Humans acquire
infection from environmental sources. Risk factors for infection include:
Male sex,
Advanced age,
Cigarette smoking,
COPD,
Organ transplants,
Malignant disease.
Diagnosis: May be difficult – X-Ray features and clinical features overlap with those of
acute bacillary pneumonias. However, hyponatraemia may be present in 30-50% of patients
and there may be CNS manifestations (especially confusion) and GIT symptoms (such as
nausea and vomiting). For definitive diagnosis – can do sputum smears and cultures –
difficult – so we rely on a urinary antigen test.
Treatment: Erythromycin ± Rifampicin. Quinolones sometimes useful.
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Note: In cases of community acquired pneumonia, when there is some doubt about the
causative organism, it is recommended that the patient should be covered with a -lactam
antibiotic (e.g. Augmentin) and a macrolide (e.g. Erythromycin).
CHLAMYDIA PNEUMONIAE: is an obligate intracellular bacterium. Can cause a mild
pneumonia but the course may be protracted with symptoms persisting for 3-6 weeks. Sore
throat, hoarseness and URT symptoms may be present. Chest X-Ray signs are similar to
those in M. pneumoniae infection. The organism is difficult to culture so one has to rely on
serologic methods for diagnosis.
Treatment: Tetracyclines appear to be superior to erythromycin. The newer macrolides
and quinolones may have more activity against the organism.
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