Pathology Notes

Clostridium difficile Updated: 02/03/2024 © Jun Wang, MD, PhD   General features Gram-positive, anaerobic, sporogenic bacterium May be part of normal colonic flora Most common cause of pseudomembranous colitis Most commonly nosocomial infectious diarrhea in the U.S. Colitis due to overgrowth and exotoxin production Results of interruption of normal colonic flora by antibiotics, chemotherapy or immunosuppression, etc Pathogenesis Disruption of normal colonic flora Colonization of C. Diff Production of exotoxins Toxin A: Enterotoxin, mucosal injury, fluid loss and inflammation, granulocyte attractant Toxin B: Cytotoxin, cytopathic Key clinical features Fever, abdominal pain and cramping Green foul-smelling diarrhea May perforate and cause septic shock Colonoscopic findings Colonic yellow plaques and nodules Pathologic findings Volcano or mushroom-like eruption of fibrin, mucin and inflammatory cells Diagnosis History of hospitalization and antibiotics

Vibrio Cholerae Updated: 02/19/2024 © Jun Wang, MD, PhD   General features G-negative, facultative anaerobe and highly motile comma-shaped bacteria Lives in warm brackish water Copepods or shellfish in contaminated water Higher risk after natural disaster Human carriage may persist after untreated infection Key clinical features Rice-water stools with tremendous fluid loss ( Thin watery with flecks of mucus ) Hypovolemic shock if not treated Pathogenesis Attachment to intestinal mucosa Motility Mucinase Toxin co-regulated pili (TCP) Cholera enterotoxin (choleragen): similar to E. coli LT Activation of adenylate cyclase Increased cAMP Efflux of Cl – and H 2 O Diagnosis Presumptive diagnosis in patients with severe diarrhea Confirmation Isolation of v. cholerae from stool culture Grow on thiosulfate citrate bile sucrose agar or taurocholate tellurite gelatin agar Antigen detection Molecular testing Darkfield microscopy Management Adequate IV Fluid and

Shigella Updated: 02/03/2024 © Jun Wang, MD, PhD   General features G-negative rods, non-motile, noncapsulated, facultatively anaerobic Highly virulent Leading cause of diarrheal death, with most common in south Asia and sub-Saharan Africa 4 groups: S. dysenteriae, S. flexneri, S. boydii, S. sonnei Key clinical features Fecal-oral Transmission Severity depends on age of patient and the strain S. dysenteriae type 1 with toxin most severe Fever (generally >101.0°F) Lower abdominal cramps; tenesmus; multiple scanty, bloody, mucoid stools Diarrhea: first watery, then bloody with WBCs Pathogenesis : Invasive but rarely causes septicemia Invade submucosa through M-cells (Microfold cells over lymphoid aggregates) Proliferate in macrophage Invade the basolateral side of colonic epithelial cells Polymerize  actin “jet trails” to spread laterally Endotoxin triggers inflammation Exotoxin Produced by S. dysenteriae, type 1 Similar to EHEC toxin, causing hemolytic uremic syndr

Salmonella enterica Updated: 02/23/2024 © Jun Wang, MD, PhD   General features Second most common cause of bacterial gastroenteritis G-negative, facultative anaerobic rod with flagella Culture on Hektoen agar (HE), catalase-positive, oxidase-negative, H 2 S production Commonly associated with chicken consumption Key clinical features Fever , vomiting and diarrhea Usually watery diarrhea Bloody diarrhea uncommon May cause sepsis Pathogenesis Endotoxin only Invasion from M cells of Peyer Patches to lamina propria  Loose diarrhea due to activation of mucosal adenylate cyclase and increased cAMP Diagnosis Suspected if acute diarrhea, with fever or in the setting of a community outbreak Culture on selective media Molecular testing Management Non-invasive gastroenteritis: self-limiting; NO antibiotics Invasive diarrhea: ampicillin, third-generation cephalosporins, fluoroquinolones, or TMP-SMZ   Back to Infectious gastroenteritis Back to Contents

Campylobacter Updated: 02/03/2024 © Jun Wang, MD, PhD   General features Most common cause of bacterial diarrhea in the US Two significant species: C jununi, C coli G-negative curved rods with polar flagella ( “gulls’ wings” ) Oxidase-positive, Catalase positive Sensitive to gastric acid, posting a higher risk in patients with reduced gastric acid production, such as autoimmune gastritis Invasion of mucosa facilitated by flagella, high molecular weight plasmids, superficial adhesins, and chemotactic factors Fecal-oral transmission, commonly associated with poultry Invade intestinal mucosa Key clinical features Abrupt onset of abdominal pain and inflammatory diarrhea Commonly self-limited, lasting 3-5 days Rarely severe colitis with toxic megacolon Serotype O:19 may be associated with Guillain-Barre syndrome Cross-reactivity with neural glycosphingolipids Reactive arthritis Diagnosis Culture: Campylobacter or Skirrow agar at 42.0°C  Management Fluid replacement E

Giardia intestinalis Updated: 01/27/2024 © Jun Wang, MD, PhD   General features Previously known as G lamblia or G duodenalis Waterborne, foodborne, or fecal-oral transmission May be asymptomatic, or presents with acute or chronic fatty, foul-smelling diarrhea   Life cycle Key clinical features Acute giardiasis: Usually watery diarrhea, nausea, etc Chronic giardiasis: May follow acute infection, may have profound weight loss, GI manifestations include loose stools, malabsorption, weight loss, abdominal cramping, etc F atty, foul-smelling diarrhea due to malabsorption Pathological and lab findings Kite and pear shaped trophozoites , in duodenum and jejunum Cyst and trophozoites in stool samples Diagnosis Antigen detection assays  Polymerase chain reaction assays Stool microscopy Management Antibiotics (metronidazole, tinidazole, nitazoxanide) Symptomatic management   Back to Infectious gastroenteritis Back to Contents

Entamoeba histolytica Updated: 01/26/2024 © Jun Wang, MD, PhD   General features A protozoan transmitted by ingestion of amebic cysts   Fecal-oral transmission usually through food or water Most cases asymptomatic, while up to 100k death annually  Life cycle Key clinical features Intestinal amebiasis and extraintestinal manifestations Bloody diarrhea due to colonic tissue damage Presentation depends on locations of infection Gastrointestinal: Gradual onset, fever, abdominal pain, tenesmus, diarrhea (with or without blood), dysentery Liver: Abscess, most common extraintestinal complication; fever, right upper quadrant pain, hepatomegaly with hepatic tenderness; may rupture and involve surrounding structures Respiratory tract: Rare, atelectasis and pleural effusions Brain: Abscesses, very rare, sudden onset symptoms such as headache, vomiting, and mental status changes with rapid progression to death Colonoscopic