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Clostridium Difficile Infection


OVERVIEW OF Clostridium Difficile Infection :

The causative agent is the bacterium called Clostridioides difficile


STRUCTURE of Clostridium Difficile Infection :

Clostridium are anaerobic motile bacteria which are ubiquitous in nature that is more common in soil. Under the microscope, they appear as long, irregular often drumstick or spindle shaped cells with a bulge at their terminal ends. They are gram positive bacteria which shows optimum growth on blood agar at human body temperatures in the absence of oxygen. When any triggering factors arises the bacteria produces spores that are able to tolerate the extreme conditions that the active bacteria cannot tolerate.

Pathogenic C.difficile strains produce multiple toxins. The toxins produced by the clostridium includes the entertoxin (Clostridium difficile toxin A) and cytotoxin(Clostridium difficile toxin B) which might result in diarrhoea and inflammation of the bowel in the infected person.

Treatment with antibiotic od clostridium might be difficult due to both antibiotic resistance and physiological factors of the bacteria. The physiologic factors include spore formation and protective effects of pseudomembrane.


CAUSES :

Taking antibiotics especially a long course of broad spectrum antibiotics

Prolonged hospitalized patients

Older adults

Colonal problems such as the inflammatory bowel disease

Having a previous history of gastrointestinal surgery

Having a weakened immune system

Having chronic kidney or liver disease

Taking proton pump inhibitors

Prior to the C.difficile infection

Walking in bare foot might in the untidy areasi ncreases the chacnces of C.difficile infection

 


PATHOPHYSIOLOGY :

The main thing that take part in the pathogenesis of Clostridium includes A)Microbial suppression

B) Collateral damage C) Window of Vulnerability.

The first phase involves suppression of the normal protective intestinal microbiota. This can occur as a result of antibiotics such as clindamycin, ciprofloxacin, cephalosporin, and fluoroquinolones. Subsequent ingestion of C difficile, which is ubiquitous, leads to germination of C difficile spores and growth of toxin-producing cells that change the gastrointestinal epithelium and invoke an immune response, leading to CDAD symptoms—the collateral damage.

The composition of normal intestinal microbiota confers multiple benefits, including supplementary vitamin production, metabolic activities, colonization prevention, and immune response stimulation.

Disruption of the intestinal microbiota leads to decreased competition for limited resources and increased bacterial cell lysis, leading to release of consumable carbon sources. Bacteria in this fixed environment can become quite complex. This has been observed in C difficile infection, in which toxin C brings the bacteria into closer contact with the epithelium, possibly for a competitive advantage or to protect a food source.

The third phase of C difficile pathogenesis is called as the period of window of vulnerability. This occurs as a result of the C.difficile treatment.

Antibiotics used for C.difficile suppresses the both the C.difficile and the endogeneous protective flora. The period of vulnerability starts at the time of the subinhibitory levels of the clostridium difficile antibiotics and ends with recovery of the intestinal microbiota. The spores in the gastrointestinal tract survive despite treatment with the antibiotics. Until the normal  gut flora microbiota, causing recurrence. Upon spore germination, toxin production from vegetative cells starts the cycle of clostridium dificile symptoms and the need for treatment with clostridium difficile antibiotics.


ROUTES OF TRANSMISSION :

Clostridium difficile is transmitted from person to person by the fecal oral route. The bare foot walk in unhygienic areas might result in entry of the organisms.The organisms forms heat resistant spores that are not killed by alcohol based hand cleansers or routine surface cleaning. Once when these spores are ingested this acid resistance capacity of the bacterium allows them to pass through the stomach unscathed.when they are exposed to the bile acids they germinate and multiply as vegetative cells in the colon.


COMMON CLINICAL SIGNS AND SYMPTOMS :

Diarrhoea

Fever

Increased bowel movements

Loss of appetite

Stomach tenderness

Nausea

Blood or pus in the stool


DIAGNOSTIC :

Stool test:

This is the simplest way to detect C.difficile is through a stool test. The stool is collected in a sterile container and it is given to the pathologist for examination.

 

Blood test:

A blood reveals the highest levels of white blood cells, a sign of infection. Very high levels can signify a more severe clostridium difficile infection in which the person might have the watery diaarhoea, intense stomach cramps and dehydration.

 

Colonoscopy or Sigmoidoscopy:

 

If you have severe symptoms of C. difficile, a physician may examine the colon using a colonoscopy or sigmoidoscopy. In both procedures, a thin, flexible tube with a light on the end is inserted through the rectum, allowing a doctor to view the colon.

A colonoscopy enables a doctor to examine the entire colon and rectum, whereas a sigmoidoscopy allows him or her to view only the rectum and the lower part of the colon.

These tests can indicate whether inflammation is present, indicating a C. difficile infection. They also allow a doctor to take tissue samples, if necessary, to further test for infection.

CT Scan

A CT scan uses X-rays and a computer to create three-dimensional, cross-sectional images of the body. If a doctor suspects you have a complication of C. difficile infection, such as a hole in the intestines, he or she may order a CT scan. Your doctor may give you a contrast agent before the scan to enhance the images. It can be taken by mouth or as an injection into a vein.

 

Polymerase Chain Reaction:

This can detect the presence of C.difficile toxin B gene in a stool sample and it is highly sensitive and highly accurate test.

 

GDH/EIA:

It uses a glutamate dehydrogenase (GDH) test in conjunction with an enzyme immunoassay (EIA) test. GDH is a very sensitive assay and can be accurately rule out the presence of clostridium difficile.

 

Enzyme immunoassay:

The enzyme immunoassay (EIA) test is faster than the other test and it is the sensitive test. This test has many infections and has a higher rate of falsely normal results.

 

Cell cytotoxicity assay:

A cytotoxicity view for the effects of the clostridium difficile toxin on human cells grown in a culture. This type of test is very much sensitive. It requies 24-48 hours for the test results to arrive.


TREATMENT AND PROGNOSIS :

Antibiotics:

Vancomycin, Fidamoxin, Metronidazole are used to reduce the infection.

 

Surgery:

The people suffering from severe pain, organ failure, toxic megacolon or inflammation of the lining of the abdominal wall, surgery to remove the diseased part of the colon.

 

Feacal microbiota transplant:

 It is also known as the stool transplant, the faecal microbiota transplant is emerging as an alternative treatment for treating recurrent C.difficile infections.FMT restores healthy intestinal bacteria by placing another person’s stool in your colon through a colonoscope or nasogastric tube. Donors blood is screened for any infections.

 

Probiotics:

Probiotics are organisms, such as bacteria and yeast, and are available over the counter. The role of these products in C. difficile infection is controversial. Research hasn't consistently shown that currently available products are helpful in preventing or treating infection with C. difficile. Advanced probiotics are currently being studied for their potential use in C. difficile treatment or prevention but aren't currently available.


PROGNOSIS :

The prognosis is good with the clostridium infection.

The fever might get subside within 2-3 days and bowel symptoms might take atleast 1 week to turn into normal.


PREVENTION :

Practice good hand hygiene

Make sure your surrounding areas are kept clean

Avoid contaminated areas.

 


Medicines used in the Treatment :

Vancomycin,

Fidamoxin,

Metronidazole