Katharine Buzzbee is a pleasant young girl of 9 years old. She was brought to the health center with complaints of sore throat with difficulty swallowing. Her mother states that Katharine has had similar symptoms three separate times this year. The illnesses begin with irritation in the throat that progress to pain. The pain radiates to her ears and she generally develops a fever during the course of each attack. The patient also has a history of developing frequent colds where she experiences headaches, a stuffy nose and frequent sneezing. Her older brother and sister have both recently had the common cold. The patient is otherwise healthy with no major illnesses or injuries.
Clinical manifestations: On examination, Katharine’s palatine tonsils are swollen, red and surrounded by exudate. She has a temperature of 101.1°F and complains of a “running nose” and headache. She appears tired and isn’t as energetic as in our previous encounters.
Diagnosis: acute tonsillitis. Throat culture confirmed strep. bacterial infection.
Etiology: Acute tonsillitis is generally caused by a viral infection1, most commonly caused by common cold viruses such as: adenovirus, rhinovirus, influenza, coronavirus, respiratory syncytial virus. The Epstein-Barr virus, herpes simplex virus, cytomegalovirus and HIV occasionally manifest as tonsillitis.
The second cause of acute tonsillitis is bacterial1 (about 30% of patients). The common bacterium is group A Beta hemolytic streptoccal. Other strains of bacteria are less common. The patient listed above has this type of infection.
Pathogenesis: virus or bacteria attacks tonsil tissue exiting the response of innate immunity and adaptive immunity of T and B cells contained in the tonsils. The lymphocytes fight the infection, which leads to inflammation. As long as the lymphocytes and other cells can weaken the virus/bacteria the damage to the cells within the tonsils will remain reversible.
Treatment: 10-day course of oral penicillin2, rest and hydration.
Prognosis: symptoms should resolve during course of treatment. If frequent onset of tonsillitis continues tonsillectomy may be recommended.
The bacteria is ingested or inhaled and attaches to the palatine tonsils (injury). At the gross level the tonsils become swollen with erythema causing pain and difficulty completing normal tasks such as swallowing.
In the study by Liljaa, Raisanenb and Stenfors3, the researchers studied bacterial and epithelial cells from palatine tonsils of nine patients with positive streptococcus pyogenes infection. The reported findings showed, “S. pyogenes could be identified both in the mucous layer covering the tonsils and attached to the surface epithelial cells. Long chains of coccus-shaped bacteria could be seen encroaching on the epithelial cell borders. S. pyogenes can apparently penetrate the mucous barrier, attach to the epithelial cells, spread from cell to cell and possibly penetrate into the outermost layer of the epithelial cells. These events in turn provoke cytokine production and/or complement activation, which induce inflammatory reaction in the tonsillar tissue (activation).”
Dead bacteria and bacterial debris will remain at the site of the infection and must be removed (phagocytosis) from this area by neutrophils and macrophages5.
Once the bacterium has been removed through phagocytes the tonsillar tissue will resume its normal form through resolution (healing process). Swelling and pain will cease.
Chronic inflammation: Ulcerative Collitis
Jedediah Jones is a 24-year-old student pursing a degree in chiropractic medicine. He presents today with abdominal pain and frequent diarrhea containing mucus and blood. The onset of these symptoms began 2 months ago, but Jedediah decided to seek treatment when his frequent bowel movements began to disrupt his studies. Patient states that on average he has approximately 8 bowel movements per day, most frequently occurring after a meal. His abdominal pain is most severe before a bowel movement, but remains constant at the pain level of 4 out of 10. Patient says pain is 6 out of 10 at its worse. Patient attributes the symptoms to his newly adopted diet mostly consisting of fast food. Until recently he lived at home where all his meals were homemade.
Patient has experienced an increased level of stress since beginning his studies (6 months ago) and subsequently quit smoking cigarettes. Patient exercises regularly, but has experienced a decrease in energy levels since the onset of symptoms. Patient denies other illness or injuries and is currently not taking any medication. Patient’s twin brother was recently diagnosed with Crohns disease and his maternal grandfather died of colon cancer at 48 years old.
Clinical manifestations: LLQ tender upon palpation and entire abdomen appears distended. Patient claims 8 bowel movements per day with a watery consistency containing mucus and blood. Conjuctiva and finger nail beds appear pale.
Diagnosis: ulcerative colitis, confirmed by positive biopsy removed during sigmoidoscopy. Inflammation of bowel appeared to extend no further than the descending colon with most severe inflammation and ulceration in the sigmoid section. Stool cultures ruled out parasitic infection.
Etiology: the cause of ulcerative colitis is unknown, but factors such as genetics7, psychological stress, smoking cessation and poor diet have been attributed to onset of disease.
Pathogenesis: as stated in the pathology textbook7, “Most investigators believe that [ulcerative colitis and Crohn disease] result from a combination of defects in host interactions with intestinal microbiota, intestinal epithelial dysfunction, and aberrant mucosal immune responses.”
Treatment: Sulfasalazine 2 pills by mouth, 3 times per day.
Rowasa (mesalamine) rectal suspension enema, at bedtime until bleeding stops.
Prognosis: continue medication until symptoms have resolved completely. Maintenance therapy will be recommended indefinitely to avoid relapse.
Podolsky8 explains in his article that inflammatory bowel disease (IBD) is believed to be the result of an ongoing activation of the mucosal immune system. This abnormal response is likely due to the defects in both the intestinal epithelium and the mucosal immune system (injury).
Podolsky8 clearly defines the inflammatory response of IBD, “Chronic, recurrent intestinal inflammation appears to result from stimulation of the mucosal immune system by-products of commensal bacteria in the lumen. Stimulation may occur as a result of the penetration of bacterial products through the mucosal barrier, leading to their direct interaction with immune cells, especially dendritic cells and lymphocyte populations (chemotaxis). Alternatively, bacterial products may stimulate the surface epithelium, possibly through receptors that are components of the innate immune-response system; the epithelium can, in turn, produce cytokines and chemokines that recruit and activate mucosal immune cells (transmigration).”
Cellular changes occur in ulcerative colitis as the chronic inflammation may lead to mucosal atrophy7, damage to the muscularis propria and disrupt neuromuscular function leading to colonic dilation and risk of perforation (cellular changes).
As stated in the textbook7, “The inflammatory process is diffuse and generally limited to the mucosa and superficial submucosa. Submucosal fibrosis, mucosal atrophy and distorted mucosal architecture remain a residual of healed disease but histology may also revert to near normal after prolonged remission (healing process).”
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