Pharyngitis

Causative agents

Common

• Acute pharyngitis, whether febrile or not, is generally caused by viruses.
  • In enteroviral infection (herpangina)
  • adenovirus infection (pharyngoconjunctival fever) 
  • Epstein-Barr virus infection (infectious mononucleosis)
• Group A B-hemolytic Streptococcus is the only common bacterial causative agent and except during epidemics it accounts for probably fewer than 15% of cases.

Rare

• Mycoplasma and Arcanobacterium hemolyticum 
• Corynebacterium diphtheria
• M mixture of anaerobic bacteria and spirochetes
• Neisseria gonorrhoeae infection

• Group A streptococcus (Scarlet fever) 
• Arcanobacterium hemolyticum
• Corynebacterium diphtheria
• Anaerobic pharyngitis (vincents angina)
• Adenovirus
  • Espstein-Barr Virus

Agents that cause exudative pharyngitis associated with rash

• Group A streptococcus (Scarlet fever) 
• Arcanobacterium hemolyticum
• Espstein-Barr Virus

When to suspect rare etiology

• Mycoplasma 
  • Associated with pneumonia
• Corynebacterium diphtheria
  • unimmunized
  • low socioeconomic groups
  • Membrane in throat
• Anaerobic bacteria and spirochetes
  • Foul odor
• Neisseria gonorrhoeae infection
  • Sexually active age group
  • Homosexuals

Transmssion 

• The common etiologic agents are spread by respiratory droplets and via contaminated hands.
• Food-borne outbreaks of streptococcal disease can occur.
• Kissing and transfer of infected saliva in infectious mononucleosis
• Oral sex with Neisseria gonorrhoeae infection

• Viral infections
  • With respiratory virus infections, such as adenovinis and coxsackie virus, there is evidence that direct invasion of pharyngeal mucosa occurs.
  • The usual pathologic changes occurring in viral pharyngitis are edema and hyperemia of the tonsils and the pharyngeal mucous membrane.
  •  An inflammatory exudate may be present with adenovirus and EBV virus infections; with the latter, nasopharyngeal lymphoid hyperplasia also occurs.
• Streptococcal infection
  • The events leading to invasive streptococcal infection of the pharymx and tonsil are also not well understood. 
  • Pharyngeal carriage of S. pyogenes is commonly observed in asymptomatic people. 
  • Factors that influence the balance between colonization and invasive infection may include natural and acquired host immunity and interference among the bacteria present in the oropharynx. 
  • Streptococcus pyogenes elaborates a number of extracellular factors, including erythrogenic toxin, hemolysins, streptokinase, deoxyribonuclease, proteinase, and hyaluronidase, which are of known or possible pathogenic importance. Certain M serotypes (1,2,4, and 12) of streptococci have been most frequently isolated from patients with uncomplicated pharyngitis, and others (1,3, and 12) from patients with serious invasive infection. 
  • Scarlet fever results from infection with a streptococcal strain that elaborates streptococcal pyrogenic exotoxin (erythrogenic toxin). Toxin production is dependent on lysogeny of the infecting streptococcus by a temperate bacteriophage.

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, but where an etiologic diagnosis is not possible on clinical grounds alone.

• Streptococcal pharyngitis.
  • Throat culture  (48 hours) is the preferred method for diagnosing streptococcal pharyngitis.
  • Rapid streptococcal  antigen screen  (45 minutes) is  highly specific but the sensitivity is approximately 85%.
  • Serum antibody titers do not rise until convalescence and are thus of no help in short-term management.
• Infectious mononucleosis.
  • Heterophile antibody test (monospot test) is used to diagnose suspected infectious mononucleosis.
• Diphtheria
• Neisseria gonorrhoeae

•  Rheumatic fever
  • occurs in about 3% of times following Streptococcal pharyngitis.
  • is a non-suppurative sequela of Streptococcus pyogenes infections. 
  • It occurs approximately 3 weeks after streptococcal pharyngitis
  • M protein has been found to be antiphagocytic and it also has epitopes which are antigenically similar to one found in the cardiac myosin and sarcolemmal membrane proteins.
  • Acute RF is thought to be an auto-immune disease.
  • Antibodies directed against M protein cross-react with cardiac tissue. 
  • These antibodies bind to the cross-reactive antigens in muscle and damage the muscle tissue. Other group A strep antigens may also cross-react with other cardiac antigens causing damage to the heart valves. 
• Acute glomerulonephritis 

are late complications of streptococcal infection and are related to immunologic response to group A streptococcal, infection.

Strategy for pharyngitis therapy

Since even exudative tonsillitis is usually of viral origin, for which there is no specific therapy, the use of antibiotics should be guided by the results of antigen detection tests or cultures, unless there are strong clinical and epidemiologic grounds to suspect a streptococcal infection.

Therapy of Streptococcal pharyngitis 

• Oral penicillins, cephalosporins, erythromycin and clindamycin are effective against Group A streptococcus.
• Sulfonamides are ineffective against group A streptococcal pharyngitis.
• Streptococcal pharyngitis is best treated orally with penicillin (125-250 mg of penicillin V three times daily for 10 days). 
• This usually produces prompt clinical response with defervescence within 24 hr. and shortens the course of illness by an average of 1.3 days.
• Administration of a single intramuscular injection of 600,000 - 1.2 million units of benzathine penicillin G is a satisfactory alternative.
• A streptococcal carrier is not at risk for rheumatic fever, is unlikely to transmit infection, and does not require treatment unless there is a history of rheumatic fever in the patient or a sibling. 
• A few children require antibiotic prophylaxis against streptococcal. disease, such as those with past history of rheumatic fever.
• In penicillin allergic patients, erythromycin is the therapy of choice.
• Symtomatic therapy (Tylenol, Fluids and electrolytes)
• Complications ( Acute glomerulonephritis, Carditis etc)

• Decrease duration of symptoms
• The primary rationale for detection and treatment of streptococcal pharyngitis  is to prevent the subsequent development of rheumatic fever. Treatment of group A streptococcal pharyngitis as long as 9 days after onset is still effective in the prevention of rheumatic fever.
• There is no convincing evidence that treatment affects the incidence or severity of acute glomerulonephritis.