Inflammatory Enteritis
Camplyobacter jejuni (Clinical Manifestations)
Associated with Guillian Barrer Syndrome (nerological autoimmunity)
Shigella (Clinical Manifestations)
Fever Feces - Frequent, painful, low volume bloody diarrhea - WBC - Mucus Abdominal Cramps Systemic effects - Kidney microvasculature --> Hemolytic-uremic syndomre (HUS) - Red cell lysis --> anemia
Helicobacter pylori (Virulence Factors)
Escapes stomach acid, resides below mucus layer. ' Urease converts urea to ammonia (basic) Type IV secretion system exports cytotoxin
Helicobacter pylori (characteristics)
Curved gram-negative rod 40-80% of adults colonized
Helicobacter pylori (Treatment)
Surgery, stress relief, antacids. Uclers often reoccur Antibiotics + bismuth salt (Pepto-bismol) + proton pump inhibitor to reduce gastric acid, speed healing
Helicobacter pylori (Identification)
- Gastric Biopsy - "Breath test" - radioactive urea --> look for radioactive metabolite - Stool antigen assay
Helicobacter pylori (Clinical Manifestations)
--Associated with MALT lymphoma --Chronic infection of gastric mucosa --Chronic infection/inflammation: stomach cancer, gastric lymphoma
Non-typhodal salmonella (Virulence Factors)
--Exit lumen via M cells (specialized epithelial cells of the mucosa-associated lymphoid tissue), invade enterocytes, mutiply locally --Induce apoptosis in macrophages via Type III system
Camplyobacter jejuni (Characteristics/Sources)
Campy= curved "Gullwing" morphology on gram stain Found in chickens
Non-typhodal salmonella (Sources)
Found in all vertebrates - Mainly from meat, eggs
Shigella (Characteristics/Sources)
Four species defined by O-antigen: S. dysenteriae (least common, most virulent), S. flexneri, S. boydii, S. sonnei (most common, least virulent) Human to human transmission
Non-typhodal salmonella (Clinical Manifestations)
Gastroenteritis (=Enterocolitis) Non-bloddy diarrhea, fever, nausea, vomiting
INFLAMMATORY ENTERITIS (Characteristics/ Clinical Manifestations)
Gram Negative Rods Bacteria invade and kill enterocytes: induce their own phagocytosis via Type III system Diarrhea, often bloody --> local production of inflammatory mediators by enterocytes and neutrophils WBC in feces Fever
Shigella (Virulence Factor)
Shiga toxin AB5 structure. A subunit cleaves RNA of large ribosomal subunit at specific position --> ribosome is inactive --Isolates without toxin produce dysentery but less severe --major role of toxin is systemic: HUS (hemolytic-uremic syndrome) - microvascular damage in kidney, red cell lysis
