Case 1

1. What are the microbial causes of pharyngitis? 

•  Acute pharyngitis, whether febrile or not, is generally caused by viruses. 
• In enteroviral infection (herpangina), adenovirus infection (pharyngoconjunctival fever) and Epstein-Barr virus infection (infectious mononucleosis) pharyngeal involvement may be prominent.
• 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.
• Mycoplasma and Arcanobacterium hemolyticum may also cause pharyngitis.
• Corynebacterium diphtheria, although infrequent, outbreaks of diphtheria are likely to occur among unimmunized, low socioeconomic groups.
• Pharyngeal infection with a mixture of anaerobic bacteria and spirochetes, while uncommon, still occurs.
• Pharyngitis is one of the several extragenital manifestations of Neisseria gonorrhoeae infection.

2. List the causative agents of exudative pharyngitis. Which of these agents may cause rash?

3. How are the agents transmitted? 

• The common etiologic agents are spread by respiratory droplets and via contaminated hands.
• Food-borne outbreaks of streptococcal disease can occur.

4. What is known about the pathogenesis of infection? 

• 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.
• 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. 
• However, epidemiologic analyses of disease association and geographic prevalence have suggested strain associated virulence rather than virulence broadly related to given serotype.
• 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.

5. How is the specific diagnosis established? 

• 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.
• Throat culture is the preferred method for diagnosing streptococcal pharyngitis.
• Rapid streptococcal tests are 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.
• Heterophile antibody test (monospot test) is used to diagnose suspected infectious mononucleosis.

6. What antimicrobial agents are effective against streptococcus pyogenes, and how is streptococcal pharyngitis treated? 

•  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.
• 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.

7. Are there any long-term consequences of streptococcal pharyngitis? 

• Rheumatic fever and acute glomerulonephritis are late complications of streptococcal infection and are related to immunologic response to group A streptococcal, infection.

8. Are late complications preventable? 

• The primary rationale for detection and treatment of GABHS 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.