Gram Negative Bacilli Flashcards
Salmonella typhi
Clinical case: A woman who recently returned from a trip to South American complains of a persistent fever, malaise, and constipation that has lasted for over a week. She recalls that the fever began slowly and climbed its way up to the current 41 degree C. A physical exam reveals that she has an enlarged spleen and a generally tender abdomen with red macules. The physician asks for a stool sample to complete the diagnosis.
Structure: rod
Reservoir: only humans
Transmission: fecal-oral; bacteria lives in the gall bladder of healthy carriers
Toxin/Pathogenesis: Vi antigen (associated with capsule) –> organism is ingested –> infection begins in ileocecal region –> organism passes through intestinal endothelial cells –> engulfed by macrophages (survive intracellularly) –> mesenteric lymph nodes and blood
Disease: at week 1, blood cultures are positive, 25% of the patients have Rose spots no abdomen/trunk, bacteria multiplies in liver, spleen –> septicemia; week 3, 85% of stool cultures are positive
-Incubation period is 5-21 days
-Symptoms include fever, headache, abdominal pain, enlargement of liver, constipation
Diagnosis: blood cultures, stool cultures, lactose non-fermentor , produces H2S gas (blackened Hektoen agar), motile, Widal test –> antibodies to O and H antigen
Treatment: fluoroquinolones or 3rd generation cephalosporins, oral vaccine, parenteral vaccine (Vi capsular polysaccharide) –> recommended for those traveling to endemic areas
Escherichia coli
Clinical case: A series of patients in a small town visit the hospital complaining of blood diarrhea, fatigue, and confusion. Physical exams reveal neurological deficits, and laboratory tests show anemia, thrombocytopenia, and uremia. Peripheral blood smears show fragmented RBCs, but subsequent Coombs tests are negative. After careful questioning, the doctors discover that each patient frequents the same fast-food burger joint. The physicians identify the causative agent with serological testing and stool cultures.
Structure: rods
Reservoir: human colon (normal flora), pathogenic in urethra and vagina; contaminated crops; bovine feces
Transmission: endogenous (from a person’s own normal flora), fecal-oral, maternal fecal flora; EHEC spreads through raw/undercooked beef and/or unpasteurized milk/juices
Toxins:
-Heat labile (LT) –> AB toxin –> ADP ribosylates Gs –> activates adenylate cyclase –> increase cAMP –> hypersecretion of ions and water –> watery diarrhea
-Heat stable (ST) –> activates guanylate cyclase –> increase cGMP –> decrease cotransport of NaCl into cells –> water remains in lumen –> watery diarrhea
-Shiga-like toxin –> inactivates 60S ribosomal subunit –> blocks protein synthesis –> cell death
Diseases: Gastroenteritis, UTI, neonatal meningitis, nosocomial infections, septicemia
-ETEC: adheres to jejunum, ileum epithelium but does not invade –> produce heat-labile toxin (LT) and heat stable toxin (ST) –> watery diarrhea (travelers diarrhea)
-EPEC: adhere to ileal epithelium but does not invade –> induces structural changes in mucosal cells –> flattening of intestinal villi (effacement) and malabsorption –> diarrhea, most often in children
-EHEC: adhere to colonic epithelium but does not invade –> secretes cytotoxic Shiga-like toxin (SLT 1 and 2) –> inflammation, bleeding –> dysentery (hemorrhagic colitis) –> toxin enters blood stream leading to HUS
-EIEC: adhere to colonic epithelium –> invade mucosal layer and secrete SLT 1 and 2 –> fever, inflammation, bleeding –> dysentery with leukocytes in stool sample
-EAEC: adherence to intestinal cells via aggregative adherence fimbriae –> persistent watery diarrhea
-DAEC: adheres to epithelium –> elongation of microvilli –> watery diarrhea
Diagnosis: gram negative, oxidase negative, lactose positive (green sheen on EMB and light purple on MacConkey), reduce nitrates to nitrites, facultative anaerobes, ferment glucose
Treatment: rehydration (diarrhea), penicillin, fluoroquinolones (UTI), 3rd generation cephalosporin (meningitis, sepsis)
Klebsiella pneumoniae
Clinical case: An alcoholic presents with a fever, pleuritic chest pain, dyspnea, and cyanosis. His cough produces a bloody “currant-jelly” sputum. CXR shows inflammation involving the right upper lobe with possible cavities.
Structure: bacillus, encapsulated
Reservoir:
Transmission:
Disease: community acquired lobar pneumonia –> bacteria colonizes right upper lobe –> avoids host defenses with antiphagocytic capsule –> stimulates inflammation throughout the lobe –> necrotizes tissue, forms cavities –> produces bloody “currant-jelly” sputum (thick, viscous)
Diagnosis: gram negative, oxidase negative, lactose positive, ferments glucose, facultative anaerobe, reduces nitrates to nitrites
At risk: alcoholics
Treatment: 3rd generation cephalosporins; most drug resistant microbe causing nosocomial infections
Proteus mirabilis
Clinical case: A woman returns to the doctor because of an annoying and persistent urinary tract infection. The woman’s complaint of Dysuria motivates more diagnostic tests, revealing the presence of large radiolucent stones in the urinary tract. The woman also provides several urine samples which are consistently high in pH.
Structure: bacillus
Reservoir: normal GI flora; sewage, soil
Transmission: urinary tract
Disease: UTI –> bacteria enters through urinary tract –> urease splits urea to form ammonium hydroxide, which increases pH –> precipitates ammonium magnesium phosphate, leading to struvite calculi formation (Staghorn renal calculi) –> urinary stones back-log urine and damage kidney; bacteria may spread to blood following a surgical procedure –> septic shock
Diagnosis: gram negative, swarming growth, oxidase negative, lactose negative, urease positive, facultative anaerobes, reduce nitrates to nitrites
Treatment: ampicillin
Shigella dysenteriae
Clinical case: A photographer for National Geographic returning from Thailand develops fever and abdominal cramps on the plane. By the time the plane lands, he suffers from blood diarrhea. His fever peaks at 40 degrees celcius. The doctor decides to do an endoscopy exam and makes a diagnosis on the hemorrhagic mucosa and ulcerations observed in the distal colon.
Structure: bacillus
Reservoir: always pathogenic, humans are the only natural host
Transmission: fecal-oral, person to person, flies, contaminated food/water, inadequate hand washing; outbreaks observed in daycare centers, nurseries, MSM
Toxin/Pathogenesis: Shiga toxin –> AB toxin –> B subunit binds to receptors on intestinal cells and A subunit enters cells –> cleaves 60S ribosomal subunit –> stops protein synthesis –> intestinal cells die
-Fecal-oral transmission –> small inoculum can overcome gastric acid defense –> endocytosed by colonic epithelium –> escapes endocytic vesicle –> replicates intracellularly and spreads cell to cell –> causes mucosal ulcers and bleeding –> damage to large intestine prevents fluid reabsorption –> dysentery
Disease: bloody diarrhea, HUS, seizures, reactive arthritis (Reiter syndrome)
Diagnosis: oxidase negative, lactose negative, gram negative, catalase negative, non-motile, does not produce H2S; stool cultured (Hektoen agar)
Treatment: rehydration, fluoroquinolones for severe cases
