Clostridium perfringens

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Clostridium perfringens

ETP Gastrointestinal

ETP Gastrointestinal

Anatomy of the gastrointestinal organs of the pelvis and perineum
Anatomy of the oral cavity (dentistry)
Anatomy of the pharynx and esophagus
Anatomy of the anterolateral abdominal wall
Anatomy of the abdominal viscera: Blood supply of the foregut, midgut and hindgut
Anatomy of the abdominal viscera: Esophagus and stomach
Anatomy of the abdominal viscera: Small intestine
Anatomy of the abdominal viscera: Large intestine
Anatomy of the abdominal viscera: Pancreas and spleen
Anatomy clinical correlates: Anterior and posterior abdominal wall
Abdominal quadrants, regions and planes
Development of the digestive system and body cavities
Development of the gastrointestinal system
Development of the teeth
Development of the tongue
Gallbladder histology
Esophagus histology
Stomach histology
Small intestine histology
Colon histology
Liver histology
Pancreas histology
Gastrointestinal system anatomy and physiology
Anatomy and physiology of the teeth
Liver anatomy and physiology
Escherichia coli
Salmonella (non-typhoidal)
Yersinia enterocolitica
Clostridium difficile (Pseudomembranous colitis)
Enterobacter
Salmonella typhi (typhoid fever)
Clostridium perfringens
Vibrio cholerae (Cholera)
Shigella
Norovirus
Bacillus cereus (Food poisoning)
Campylobacter jejuni
Bacteroides fragilis
Rotavirus
Enteric nervous system
Esophageal motility
Gastric motility
Gastrointestinal hormones
Chewing and swallowing
Carbohydrates and sugars
Fats and lipids
Proteins
Vitamins and minerals
Intestinal fluid balance
Pancreatic secretion
Bile secretion and enterohepatic circulation
Prebiotics and probiotics
Cleft lip and palate
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Oral candidiasis
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Ludwig angina
Warthin tumor
Oral cancer
Dental caries disease
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Gingivitis and periodontitis
Temporomandibular joint dysfunction
Nasal, oral and pharyngeal diseases: Pathology review
Esophageal disorders: Pathology review
Esophageal web
Esophagitis: Clinical
Barrett esophagus
Achalasia
Zenker diverticulum
Diffuse esophageal spasm
Esophageal cancer
Esophageal disorders: Clinical
Boerhaave syndrome
Plummer-Vinson syndrome
Tracheoesophageal fistula
Mallory-Weiss syndrome
GERD, peptic ulcers, gastritis, and stomach cancer: Pathology review
Gastroesophageal reflux disease (GERD)
Peptic ulcer
Helicobacter pylori
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Peptic ulcers and stomach cancer: Clinical
Pyloric stenosis
Zollinger-Ellison syndrome
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Small bowel bacterial overgrowth syndrome
Irritable bowel syndrome
Celiac disease
Small bowel ischemia and infarction
Tropical sprue
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Malabsorption syndromes: Pathology review
Malabsorption: Clinical
Zinc deficiency and protein-energy malnutrition: Pathology review
Whipple's disease
Appendicitis: Pathology review
Appendicitis
Appendicitis: Clinical
Lactose intolerance
Protein losing enteropathy
Microscopic colitis
Inflammatory bowel disease: Pathology review
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Pediatric gastrointestinal bleeding: Clinical
Abdominal pain: Clinical
Disorders of carbohydrate metabolism: Pathology review
Glycogen storage disorders: Pathology review
Glycogen storage disease type I
Glycogen storage disease type II (NORD)
Environmental and chemical toxicities: Pathology review
Medication overdoses and toxicities: Pathology review
Laxatives and cathartics
Antidiarrheals
Acid reducing medications
Kwashiorkor
Galactosemia

Flashcards

Clostridium perfringens

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Questions

USMLE® Step 1 style questions USMLE

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A 30-year-old man is brought to the emergency department with pain and discoloration of the right thigh. A week ago the patient was involved in a motor vehicle accident and suffered deep lacerations over the same region. The patient was evaluated at an urgent care facility afterward and a piece of scrap metal was removed from the right thigh. Currently, temperature is 38.9°C (102.0°F), pulse is 108/min, respirations are 14/min, blood pressure is 70/44 mmHg and SpO2 is 93% of room air. The appearance of the right thigh is shown below. On palpation of the right thigh, there is tenderness and crepitus. Which of the following toxins is most likely responsible for this patient’s presentation?
 
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Transcript

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Clostridium perfringens is from the family of Clostridia, and as a family, they’re obligate anaerobes, meaning they don’t require oxygen to thrive, in fact, they’re better off without it.

Anaerobes, clostridia included, tend to lack the enzymes catalase or superoxide dismutase, so oxygen is actually toxic to them.

In nature, they thrive in deep, compact soil, and when they feel the stress of fresh oxygenated air, they often produce spores, which are extremely resilient to the environment, and can even survive cooking.

When conditions improve, for example, when food is slowly cooled or stored, the spores can sprout into full-fledged Clostridia.

In fact, at an optimum temperature, Clostridium perfringens has one of the fastest growing rates of any bacterium! In the lab, when doing a gram stain, Clostridium perfringens is Gram-positive, or purple when Gram stained, and look like big cylinders or rods, also called bacilli.

Clostridium perfringens is a common cause of food poisoning, in fact, it’s sometimes called “the cafeteria germ”.

That’s because it typically infects food that’s prepared in large quantities, and then kept warm for prolonged periods, such as in cafeterias or buffets.

Clostridium perfringens are found in the environment and they can accidentally contaminate food when it’s been left out for a while.

If a person eats food contaminated with C. perfringens, the bacteria will soon colonize the gut.

Within 24 hours, the bacteria starts to make clostridium perfringens enterotoxin, or CPE.

The CPE specifically targets the tight junctions that connect epithelial cells lining the intestines to one another.

When the tight junctions get destroyed, it causes inflammation and compromises the structural integrity of the intestinal wall.

Fortunately, CPE is heat labile, so prolonged cooking at 72°C or above will inactivate it.

And that’s one reason why freshly cooked food is best to eat - the other reason is that it’s simply tastier that way!

But uncooked food - like salads, or reheated food - like leftovers, can be a good home to Clostridium perfringens.

The symptoms of Clostridium perfringens enteritis include abdominal cramping, watery diarrhea, and vomiting.

Fortunately, most of these improve over the course of a day, as the bacteria makes its way through the intestines.

In terms of treatment, antibiotics aren’t needed, and instead the goal is to keep the individual well hydrated.

Now, instead of getting into food, Clostridium perfringens can also sometimes get into a wound.

This can happen when wounds are made by dirty, sharp objects, that come into contact with soil that’s rich with Clostridium perfringens and other anaerobes, like gardening or farming equipment.

And if there’s a deep wound, it can cause clostridial myonecrosis.

Key Takeaways

Clostridium perfringens is a spore-forming, gram-positive obligate anaerobe bacterium that can cause food poisoning. The most common symptoms of Clostridium perfringens food poisoning are abdominal cramps and diarrhea, and vomiting. Clostridium perfringens also causes myonecrosis or gas gangrene once it gets into a wound. It can be deadly unless urgent surgical debridement and antibiotic therapy are initiated rapidly.