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wrote...
13 years ago
Case 1 (3)
A 35-year old man had not been feeling well for a few days with nonspecific aches and pains in his joints and a slight headache.  He attributed  this to a barbecue he had attended a few days previously, where he also drunk a considerable amount of alcohol. The following day he felt considerably worse with severe colicky abdominal pain, and  bloody diarrhea,  going to the bathroom 10 times during the day. This persisted overnight and he went to the local E.R. On examination he was noted to be dehydrated and rather pale. He was admitted to the hospital for intravenous rehydration,  and blood and fecal  samples were sent for culture. He was started on antibiotics, and over the subsequent days he improved with lessening of the symptoms and was discharged home. Some weeks later he began to develop weakness in his feet, which gradually affected his legs. He contacted his primary care physician who admitted him to hospital.  Over the subsequent few days,  the paralysis affected his upper leg muscles, and gradually over the ensuing weeks slowly resolved with treatment.  Fecal culture on selective medium incubated at 42 C in a microaerophilic environment revealed a small, oxidase positive colony that Gram stained revealed to be a small, curved/gullwing Gram negative  rod.
1.What is the causative agent? (Genus and species, no abbreviation)

2. What is the disease pathogenesis?
   
3. How is the disease treated?








Case 2 (5)
An elderly lady, of no fixed abode, arrived at the hospital’s E.R. after having fallen. She was admitted for fixation of a  hip fracture .  Shortly after admission she developed signs of a chest infection and was started on a cephalosporin, which she remained on for a week. Subsequently she developed profuse watery diarrhea and abdominal pain. A feces sample was sent to the laboratory to test for the toxins of Clostridium difficile, which proved positive and she was commenced on oral vancomycin. Despite treatment,  the diarrhea persisted and it also failed to respond to a course of metronidazole. The condition of the patient worsened and a sigmoidoscopy was performed, revealing that she had pseudomembranous colitis. Her clinical condition deteriorated and she developed toxic megacolon and an emergency colectomy was performed. The patient died shortly after the operation.
1.What are the two exotoxins  of Clostridium difficile,  AND  how are they responsible for disease in question?
a.

b.

2.  Summarize these  characteristics of C. difficile:  selective medium, atmosphere for in vitro growth, and Gram stain result.

3.How is the disease diagnosed  (methodology) typically when searching for the organism’s toxins in stool?









Case 3 (12)
   A 50-year old advertising executive consulted his primary health-care provider because of tiredness, lethargy, and an abdominal pain centered around the lower end of his sternum, which woke him in the early hours of the morning. The pain was relieved by food and antacids. His uncle died of stomach cancer and he was worried that he had the same illness. On examination his doctor noticed that he seemed a bit pale and that he had a tachycardia. His blood pressure was low. He was slightly tender in his upper abdomen but there was no guarding or rebound tenderness.  The doctor took blood and feces samples and organized for an upper gastrointestinal endoscopy. The full blood count showed a hypochromic normocytic anemia with a hemoglobin of 8.9 consistent with iron-deficiency anemia. The gastroscopy showed a 3 cm ulcer in the prepyloric region of the stomach.  The patient was started on routine treatment for a duodenal ulcer.
1.What is the causative agent? (Genus and species, no abbreviation)

2. What is the host immunological response to the infection?

 3. How is the disease diagnosed IN the clinical laboratory?

Case  4 (22)
   A 37-year old Hispanic woman, a native of Southern Mexico, went to see her primary care physician after complaining of a persistent rash throughout her body. The woman had three children, was a nonsmoker, and appeared to be well-nourished.   Her symptoms had started 5 years BEFORE with spasms, with needle-like pain, in her arms. She also felt tired and stressed and had been initially diagnosed with depression. Her skin examination indicated atopic dermatitis and urticaria and she was prescribed ibuprofen, fluoxetine, and hydroxyzine.  Physical examination revealed numerous hypopigmented skin lesions, especially those on her arms, nasal bridge area, cheeks, abdomen, and back and her legs. Her eyebrows had started thinning and she had numbness in her forearm.  The patient had a biopsy of skin lesions on the abdomen.  Acid-fast bacilli were detected .
1.   What is the most likely causative agent? Genus and species, no abbreviation.

2.   Describe the two  (2) clinical forms of disease caused by this organism?


3.    How is the disease  managed/treated?


Case 5
A 10 year old Amish child is brought to the emergency room because of high fever and sore throat of six days duration.  Examination reveals a temp of 101. There was a dirty gray membrane over the tonsils and posterior pharynx.  History reveals, which is typical, that the child has had no infant/childhood immunizations.  Culture of the throat on cysteine-tellurite blood agar (CTBA) revealed small  gray to black colonies which Gram stained tiny pleomorphic  Gram positive rods.
1.    What is the identification of this organism? GENUS AND SPECIES.

2.    What is the relationship between this organism and the Elek test?

3.   Why are some strains of this organism pathogenic and some are not? 
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wrote...
Educator
13 years ago
First one is Campylobacter jejuni; it is typically treated with ciprofloxacin. More severe cases are treated with erythromycin, azithromycin or norfloxacin.
wrote...
Educator
13 years ago Edited: 13 years ago, bio_man
2.

- C. difficile inherent pathogenicity lies in its ability to produce toxin. In particular, this pathogen produces two potent cytotoxins, namely, toxin A and toxin B, which ultimately lead to C. difficile-associated infection and disease.

Toxins A and toxin B are glucosyltransferases that target and inactivate the Rho family of GTPase enzmyes. Toxin A induces actin depolymerization by a mechanism correlated with a decrease in the ADP-ribosylation of the low molecular mass GTP-binding Rho proteins. Another toxin, binary toxin, has also been described, but its role in disease is not yet fully understood. Eventually, this leads to the deterioration of epithelial cell components and inevitably cell death. Additionally, both toxins induce a strong cellular inflammatory reaction and mass cytokine release, as well as activate the enteric nervous system, attracting neutrophils to the site. The overall outcome of toxin A and toxin B production is colonic mucosal injury and inflammation.

- Laboratory culturing and Gram staining procedures are considered too unspecific to identify C. difficile in clinical situations due to its morphological similarity to other Clostridia species that make up the normal microflora of the colon. Typical diagnostic tests select for the presence of toxin A or toxin B production (Mylonakis et al., 2001). Tissue culture assay for specificity of toxin B cytotoxicity remains one of the most sensitive and exact tests used for diagnosis. Enzyme-linked immunosorbent assays (ELISAs) are also able to identify toxin A and/or toxin B in stool, which are rapid, specific, and most frequently used for clinical diagnosis of presumed C. difficile infections.
wrote...
Educator
13 years ago
3. Helicobacter pylori

- Inflammatory response with the infiltration of various immune cells into the infected gastric mucosa - But this is very limited.

- Diagnostic tests utilized to characterize H. pylori infection include a urease enzyme test where the infected person drinks a carbon labeled urea solution in which the bacteria can metabolize. The labeled carbon dioxide can then be detected in the breath. Another test includes a biopsy through endoscopy. The histology of the biopsy sample is analyzed for the pathogen' presence and to determine the degree of infection and damage. Other non-invasive tests include a non-quantitative enzyme-linked immunosorbent assay (ELISA) which detects H. pylori antibodies in blood serum, and by a fecal antigen test.
wrote...
Educator
13 years ago
4. Mycobacterium leprae

- Two primary forms of leprosy exist, lepromatous and tuberculoid.

- The first modern anti-leprosy drug was the sulfone derivative dapsone, which inhibits the bacterial synthesis of dihydrofolic acid, required for nucleotide synthesis. Although dapsone resistance has appeared in M. leprae, the drug is usually given in conjunction with other antibiotics. Unwanted effects are fairly frequent, a few are serious. Tuberculoid leprosy heals within months and drugs are only required for three years, while lepromatous leprosy requires lifelong treatment to prevent recurrence. The use of clofazimine for lepromatous leprosy is a dye that is given orally and can accumulate by sequestering in macrophages. Action is delayed for six to seven weeks, and its half-life is eight weeks. Unwanted effects include red skin and urine, sometimes gastrointesinal disturbances.
wrote...
Educator
13 years ago
5. Corynebacterium diptheriae

2.    What is the relationship between this organism and the Elek test?

It is used to test for toxigenicity of C. diphtheriae.

3.   Why are some strains of this organism pathogenic and some are not? 

Some strains contain the diphtheria toxin gene (these are pathogenic) while others don't contain this gene (these are nonpathogenic).
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