Clinical features & Diagnosis of Clostridium Difficile Infection.pdf
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Clostridium difficile infection (CDI) commonly presents with diarrhea, often unformed and characterized by a specific odor, with complications including fever and abdominal pain. Diagnosis requires both clinical criteria and laboratory testing for toxins, but no single test offers high sensitivity or rapid results; thus, multiple approaches may be necessary. Recurrence rates after treatment are significant, highlighting the challenge of managing CDI as it may involve either relapses or reinfections due to ongoing disruption of the normal fecal microbiota.
![CLINICAL MANIFESTATIONS & DIAGNOSIS OF CLOSTRIDIUM DIFFICILE INFECTION
Clinical Features
Diarrhea is the most common manifestation caused by C. difficile.
Stools are almost never grossly bloody and range from soft and unformed to watery or mucoid
in consistency, with a characteristic
odor.
Clinical and laboratory findings include fever in 28% of cases, abdominal pain in 22%, and
leukocytosis in 50%.
When adynamic ileus (which is seen on x-ray in ~20% of cases) results in cessation of stool
passage, the diagnosis of CDI is frequently overlooked. A clue to the presence of unsuspected
CDI in these patients is unexplained leukocytosis, with ≥15,000 white blood cells (WBCs)/μL.
Such patients are at high risk for complications of CDI, particularly toxic megacolon and sepsis.
C. difficile diarrhea recurs after treatment in ~15–30% of cases and remains one of the most
challenging treatment dilemmas. Recurrences may represent either relapses due to the same
strain or reinfections
with a new strain. Susceptibility to recurrence of clinical CDI is likely a result of continued
disruption of the normal fecal microbiota caused by the antibiotic used to treat CDI.
Diagnosis
The diagnosis of CDI is based on a combination of clinical criteria:
(1) diarrhea (≥3 unformed stools per 24 h for ≥2 days) with no other recognized cause
plus
(2) detection of toxin A or B in the stool, detection of toxin-producing C. difficile in the stool by
nucleic acid amplification
testing (NAAT; e.g., polymerase chain reaction [PCR]) or by culture, or visualization of
pseudomembranes in the colon.
PMC is a more advanced form of CDI and is visualized at endoscopy in only ~50% of
patients with diarrhea who have a positive stool culture and toxin assay for C. difficile .
Endoscopy is a rapid diagnostic tool in seriously ill patients with suspected PMC and an acute
abdomen, but a negative result in this examination does not rule out CDI.](https://image.slidesharecdn.com/clinicalfeaturesdiagnosisofclostridiumdifficileinfection-240726123616-28e2e324/85/Clinical-features-Diagnosis-of-Clostridium-Difficile-Infection-pdf-1-320.jpg)
Clinical features & Diagnosis of Clostridium Difficile Infection.pdf
- 1. CLINICAL MANIFESTATIONS & DIAGNOSIS OF CLOSTRIDIUM DIFFICILE INFECTION Clinical Features Diarrhea is the most common manifestation caused by C. difficile. Stools are almost never grossly bloody and range from soft and unformed to watery or mucoid in consistency, with a characteristic odor. Clinical and laboratory findings include fever in 28% of cases, abdominal pain in 22%, and leukocytosis in 50%. When adynamic ileus (which is seen on x-ray in ~20% of cases) results in cessation of stool passage, the diagnosis of CDI is frequently overlooked. A clue to the presence of unsuspected CDI in these patients is unexplained leukocytosis, with ≥15,000 white blood cells (WBCs)/μL. Such patients are at high risk for complications of CDI, particularly toxic megacolon and sepsis. C. difficile diarrhea recurs after treatment in ~15–30% of cases and remains one of the most challenging treatment dilemmas. Recurrences may represent either relapses due to the same strain or reinfections with a new strain. Susceptibility to recurrence of clinical CDI is likely a result of continued disruption of the normal fecal microbiota caused by the antibiotic used to treat CDI. Diagnosis The diagnosis of CDI is based on a combination of clinical criteria: (1) diarrhea (≥3 unformed stools per 24 h for ≥2 days) with no other recognized cause plus (2) detection of toxin A or B in the stool, detection of toxin-producing C. difficile in the stool by nucleic acid amplification testing (NAAT; e.g., polymerase chain reaction [PCR]) or by culture, or visualization of pseudomembranes in the colon. PMC is a more advanced form of CDI and is visualized at endoscopy in only ~50% of patients with diarrhea who have a positive stool culture and toxin assay for C. difficile . Endoscopy is a rapid diagnostic tool in seriously ill patients with suspected PMC and an acute abdomen, but a negative result in this examination does not rule out CDI.
- 2. Despite the array of tests available for C. difficile and its toxins , no single test has high sensitivity, high specificity, and rapid turnaround. # Most laboratory tests for toxins, including enzyme immunoassays (EIAs), lack sensitivity. However, testing of multiple additional stool specimens is not recommended. # NAATs (including PCR) are widely used diagnostically and are both rapid and sensitive; however, concern has been raised that PCR may detect colonization with toxigenic C. difficile in patients who have diarrhea for a reason other than CDI. # Confirmation of the presence of toxin in the stool in addition to PCR or glutamate dehydrogenase (GDH) positivity is recommended in the European CDI guidelines for diagnosis of CDI, and inclusion of a stool toxin test is recommended in the U.S. guidelines when there are no prior criteria for stool submission. Empirical treatment is appropriate if CDI is strongly suspected on clinical grounds and stool testing is delayed. # Testing of asymptomatic patients is not recommended except for epidemiologic study purposes. In particular, so called tests of cure following treatment are not recommended because >50% of patients continue to harbor the organism and its toxin after diarrhea has ceased and test results do not always predict the recurrence of CDI. The results of such tests should not be used to restrict placement of patients in long-term care or nursing home facilities. Reference : Harrison's Principles of Internal Medicine 21st edition