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147 Cards in this Set
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Nausea and Vomiting
wk 21 |
Unit 3, week 2
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Rotavirus
(basic description) |
Prolonged gastroenteritis in infants (1st most important)
deaths due to dehydration. Fecal-oral transmission. Survives well on fomites because it can withstand drying. Outbreaks occur in preschools, day care and hospitalized infants.Prone to have a FEVER with prolonged syndrome (kids sick for a week) 3 Layered capsid Icosahedral, Non-enveloped, 11 Segs of dsRNA Reoviridae Family infects non-dividing differentiated enterocytes 6 VPs and 6 Non structural NSPs |
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Important Rotavirus proteins
VP4, VP7, & NSP4 |
VP4 - protease-sensitive. Required for Viral Activation and entry into cell
VP7 - glycoprotein (outer capsid part), Acquired during a process during which particles are transiently enveloped, binds to Ca2+ NSP4 - Viral budding into the ER by binding inner capsid proteins Intracellular release of Ca leading to diarrhea Disrupts tight junctions allowing for paracellular flow of H2O and electrolytes Stimulates the enteric nervous system |
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Rotavirus
(Transmission, Immunity, & Vaccine) |
Long duration (1 week)
kids and infants (not neonates b/c they have ABs from mom transplacentally and milk), IgA and interferon Rotavirus Vaccine 1st dose at 6-14 wks, not recommended after |
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Adenovirus
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Infant gastroenteritis (2nd most important)
Resist drying ,detergents, GI acids and secretions, even mild chlorine treatment. Transmitted by fecal-oral, aerosols, fingers, fomites, and in poorly chlorinated pools. Naked deltaicosahedral Linear dsDNA Adenoviridae family E1A and E1B proteins M: adenovirus inclusions - nuclei filled w. virus and no affect on cell size (unlike CMV) |
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Adenovirus Interference w/ Host defense (3 ways)
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VA-RNA: decoy RNA, block interferon anti-viral response (which normally causes pkr protein to shut down cell protein synthesis)
E1A, E1B, E3 - promote cell proliferation & block apoptosis by binding Rb and p53 Inhibits MHC I expression |
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Norovirus (Norwalk)
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Naked capsid
(+) ss RNA Low infectious dose, Foodborne - contaminated food ie shellfish ADULT gastroenteritis Star morphology Caliciviridae family |
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Hepatitis A virus
(enterovirus) |
Naked icosahedral capsid, (+) ssRNA
Single serotype Picornaviridae family Acute, prone to outbreaks Stomach to Blood-stream to Liver:Genome has a Vpg protein that binds to receptors on liver cells. Cytotoxic Tcells req'd to eliminate infected cells, causing damage to liver Fecal-Oral transmission Acid stable Acute self limiting disease Life long immunity is established. Contagious 10d prior to symptoms arise. Incubation for 15 to 50 days prior abrupt onset of symptoms Associated with consumption of shell fish or contaminated food. DAYCARE centers are a major source of spread Immune serum globulin Prophylaxis effective Rarely fatal Vaccine: Killed HAV |
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Calicivirus
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Naked Capsid, (+)ssRNA
Single protein capsid M: cup-shaped indentions Calciviridae family |
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Astrovirus
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Naked capsid
(+) ss RNA M: star shaped Similar to Norovirus Astroviridae Family Sporadic cases and occasional outbreaks of diarrheal illness in infants, young children and the elderly. Usually resolves after 48 hours, without serious consequences. Milder ds than Rotavirus - no hospitalization |
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Enterobacteriaceae
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Family of gram (-) rods
Found in wide variety of envs (soil, water, intestine, etc) Some opportunistic pathogens; others are always human pathogens; some are normal flora that can become pathogenic after acquiring virulence genes from other sources Most are motile and facultative anaerobes LPS is the major cell wall antigen Incl: Citrobacter freudii & koseri, Enterobacter aerogenes & cloacae, E. coli, Klebsiella pneumonia & oxytoca, Morganella morganii, Proteus mirabilis, Salmonella enterica, Serratia marcescens, Shigella sonnei & flexneri, Yersinia pestis & entercolitica & pseudotuberculosis |
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Salmonella
typhoid (S. enterica Typhi) |
Host: humans
Fecal-oral route of contaminated food or water while non-typhoid serovars are passed by animal handling or improper handling of contaminated food (poultry, eggs, dairy are the most common) More severe illness than the non-typhoid serovars although luckily infection with the typhoid serovars are also less common. Sxs: Enteric fever, abdominal pain, transient diarrhrea/constipation, salmon maculopapular rash on trunk High risk areas in panama, west coast of south america, africa, india Tyhpoid Mary |
Case 5: A 3-year-old man presents with sudden-onset, crampy abdominal pain and diarrhea. The diarrhea is watery and contains mucus. The patient also complains of low-grade fever with chills, malaise, nausea, and vomiting. Careful history reveals that he had ingested partially cooked eggs at a poultry farm 24 hours before his symptoms began.
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Salmonella
non-typhoid |
Host: broad range (turtle)
Sxs: Gastroenteritis, abdominal pain, vomiting, and inflammatory diarrhrea |
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Salmonella Virulence Factors
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Fimbriae - attachment to epithelial cells of sml int; invade thru M cells (microfold) and enterocytes
Replication occurs in the endocytic vacuole; disseminated infection can occur Enterotoxin production in gastroenteritis-causing strains. Dx & Tx: Isolation from stool specimens on selective media and subsequent antibiotic susceptibility testing; Antibiotics are recommended for Typhoid serovars but not normally for non-typhoid serovars. |
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Shigella
(general characteristics) |
Gram-neg rod; non-motile
Slow lactose-fermenters (neg) Can cause dysentery Cause of shigellosis (gastroenteritis); begins in small intestine and progresses to the colon Spread fecal-oral route (low infectious dose) usually by water contaminated with human feces; not usually zoonotic Ds:Growth on selective media, serotyping based on O antigen to distinguish between groups. S.dysenteriea is Group A S. sonnei is Group D. Tx: Often self-limiting but antibiotics help significantly (preference for fluoroquinolones) |
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Shigella dysenteriae
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S. dysenteriae tends to produce more severe gastroenteritis than S. sonnei;
CP: starts as a watery stool; Infection travels down small intestine into colong stimulating ulceration and inflammation that result in fever, abdominal cramps, tenesmus, and presence of blood, mucous, and pus in stools |
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Shigella sonnei
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S. sonnei causes 85% of Shigellosis cases in the U.S. (mostly kids & male homosexuals)
CP: watery stool; Self-limiting (Sxs goes away on its own) |
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Shigella
mechanism of invasion of intestinal epithelial cells |
Shigella invades “M cells” of colon. After adherence, a Type III secretion sys induces bacterial cell uptake w/in vacuoles (no replication in vacuole).
Shigella escapes f/ vacuole, replicate w/in cytoplasm, & invades neighboring cells via a comet-like actin tail. IL-1 release & PMN migration causes further loss in cell integrity. |
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Shiga toxin of S. dysenteriae
Mechanism of Action |
can be cytotoxic, enterotoxic, or neurotoxic
AB5 toxin B subunit - imp for binding to cell surface via a glycolipid (Gb3) and subsequent internalization. A subunit - releases from the B subunit by furin (a protease), inhibits protein translation by specifically cleaving the 28S rRNA causing cellular damage to intestinal epithelium & sometimes glomerular endothelial cells. |
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Escherichia coli
General characteristics |
Gram negative rod, motile, strong lactose-fermenter
Part of normal flora but also considered opportunistic pathogen Common cause of sepsis and gastroenteritis One of the most dangerous serotypes of E.coli is O157:H7 (an EHEC) Virulence often determined by presence of plasmids or pathogenicity islands & often involves adherence factors or exotoxins Most common causative microorganism of UTIs. Only one of these five enteric categories, EAEC, is also considered to be uropathogenic. |
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Enterotoxigenic E. coli (ETEC)
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site: sml int
Ds: Traveler's diarrhea. Infanct diarrhea in developing countries; watery diarrhea, vomiting, nausea, low-grade fever Food: fruits, veggies, scallops, tuna paste, soft cheeses P/Vir factors: heat-stable, heat labile enterotoxins that stim hypersecretion of fluids & electrolytes, adhesion mediated by colonization factor antigens Dx: clinical presentation, isolation of lactose fermenting colonies, and sometimes the presence of enterotoxin in the stool. |
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Enterhemorrhagic E. coli (EHEC)
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Site: Lg int
Ds: watery diarrhea progressing to bloody diarrhea, cramps, little/no fever. Hemolytic-uremic syndrome (O157:H7) Food: undercooked beef (Jack in the Box), sausage, chicken, lunch meats, deer jerky, lettuce, radishes, alfalfa sprouts, potatoes, milk, apple juice, cider, cheese curds Dx: isolation of sorbitol nonfermenting colonies on SMAC + serotyping, and/or presence of Shiga toxin in the stool |
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Enteroinvasive E. coli (EIEC)
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site: large intestine
Ds: Dev countries, fever, cramping, watery diarrhea, may progress to dysentery w/ bloody stools P & Vir F: Plasmid mediated invasion & destruction of epithelial cells lining colon, adhesion mediated by Invasive Plasmid Antigen (IPA) Food: cheese, guac Dx: DNA probe kit; looks so similar to Shigella with other testing methods that it is often misdiagnosed |
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Entero-aggregative E. coli(EAEC)
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children as watery diarrhea, vomiting, dehydration and sometimes a UTI.
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Entero-pathogenic E. coli (EPEC)
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generally limited to young children and presents with a low-grade fever, malaise, vomiting, and diarrhea. Mucous but not blood is present in the stool.
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Sorbitol-MacConkey Media (SMAC)
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no lactose
E. coli 0157:H7; no fermentation of sorbitol on SMAC media A non-0157:H7 strain; fermentation of sorbitol on SMAC media |
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Hemolytic Uremic Syndrome (HUS)
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Caused by EHEC, most commonly O157:H7. Presents several days following the development of blood diarrhea. Oliguria and hematuria follow.
Shiga toxin damages endothelial cells resulting in activation of apoptosis, platelet aggregation, cytokine release, and vasoconstriction. Kidneys and RBC’s experience greatest damage. major cause of acute renal failure in children. Can cause permanent kidney damage or death. |
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Yersinia enterocolitica
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Gram-neg rod; intracellular pathogen
Cold tolerant (grow & survive refrigeration); problem w/ stored blood (blood transfusion-related bacteremia) Source of infection: zoonotic (pigs, rodents, livestock, rabbits); contaminated meat, milk, or water CP: gastroenteritis involving distal ileum, colon and mesenteric lymph nodes; 1-2 weeks of abdominal pain, fever, and diarrhea (often bloody). Often misdiagnosed as appendicitis (pseudoappendicitis). Infection can trigger autoimmune disorder including reactive arthritis. Labs: Lactose negative, urease positive, motility only at temperatures below 30°C. Tx: self-limiting but may require antibiotics in severe cases (responds well to a variety of antibiotics) |
CASE
28-year-old woman complains of painful swelling of R knee and and tender skin eruptions on both shins. For the past 2 weeks she has also had watery diarrhea that developed after she consumed some raw PORK. She also complains of low-grade fever and mild abdominal pain. Both red and white blood cells were observed in her stool sample. A stool sample revealed a gram-negative rod that was only motile at temperatures below 30°C. Growth on MacConkey |
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Enterobacteriaceae
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all glucose fermenters and do not produce cytochrome c oxidase
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E. coli
(lab) |
Lactose (+)
Indole (+) Citrase (-) |
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Citrobacter
(lab) |
Lactose (+)
Urease (+) H2S (+) |
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Klebsiella
(lab) |
Lactose (+)
Urease (+) H2S (-) |
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Enterobacter
(lab) |
Lactose (+)
Urease (-) |
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Proteus
(lab) |
Lactose (-)
Glucose (+) Motile Urease (+) (catheters) |
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Salmonella
(lab) |
Lactose (-)
Glucose (+) Motile Urease (-) H2S (+) |
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Serratia
(lab) |
Lactose (-)
Glucose (+) Motile Urease (-) H2S (-) pink on TSA |
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Shigella
(lab) |
Lactose (-)
Glucose (+) Non - Motile H2S (-) |
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Pseudomonas
(lab) |
Lactose (-)
Glucose (-) Oxidase (+) |
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Diarrhea
wk 22 |
Unit 3, week 3
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Food poisoning
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microorganism is ingested
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Food intoxication
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Food contaminated with a toxin
Symptoms appear sooner than those of a food poisoning. |
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Campylobacter jejuni
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Gram negative, curved/spiral rod, motile
Grows best at 42°C; considered slow-growing Requires microaerophilic conditions-decreased oxygen; increased carbon dioxide Causes significant damage to the mucosa of the Jejunum, ileum, or colon Source of infection: zoonotic (poultry, cattle, sheep); contaminated food, milk, or water Symptoms: abdominal pain, fever, 2-3 day diarrhea (with blood and pus possible) Treatment: usually self-limiting but may be treated with macrolides (usu clears itself w/in a few days, if bad need antibiotic Tx) Easily killed by gastric acids but can become a problem in those that decrease or neutralize stomach acid Linked to Guillain-Barré syndrome and reactive arthritis |
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Clostridium: C. botulinum, C. perfringens, and C. difficile
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Gram-positive rods
Strict anaerobes Endospore formers (C. perfringens-more rarely); allows survival under adverse conditions Produce numerous toxins Rapid growth rate Found in the SOIL, water, sewage Part of our normal intestinal flora |
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Foodborne botulism
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Intoxication (from canned foods in past)
caused by the germination of spores in food Symptoms develop within 1-3 days and include weakness, dizziness, blurred vision, CONSTIPATION. Neurological problems, including respiratory paralysis can become severe if not fatal. 5-15% mortality rate |
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Infant botulism
Clostridium botulinum |
most common type of botulism in U.S.;
infants 1-6 months most often affected. Common sources include soil, dust, honey, and infant milk powder. Caused by proliferation of microorganism in G.I. tract w/ toxin release. (poisoning) Sx: constipation and failure to thrive, may progress to paralysis (FLOPPY BABY syndrome). Mortality relatively low (1-2%). Tx: antitoxin; ventilatory support |
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mechanism of action of Botulinum Toxin
Clostridium botulinum |
an “A-B” toxin
“A” subunit = toxic component, endopeptidase activity inactivates proteins involved in the release of acetylcholine containing vesicles into the synapse “B” subunit = receptor binding on neurons. Result is flaccid paralysis. Example: Botox releases/relaxes fine muscles in face |
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Clostridium perfringens
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Cause of gastroenteritis and also severe soft tissue infections (gas gangrene).
Normal flora bacterium commonly found in soil and feces-contaminated water Food poisoning is observed commonly in CONTAMINATED MEAT that was not refrigerated properly. SX: include watery diarrhea, abdominal cramps (within 8-24 hours). Most often caused by “TYPE A”. The enterotoxin disrupts ion transport in the ileum leading to fluid loss. 2nd less common form of gastroenterits with a high mortality rate (50%!!!) is a NECROTIZING ENTERITIS; caused by the beta toxin of “TYPE C”. The beta toxin is a pore-forming toxin. The diarrhea is often bloody. |
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Alpha Toxin
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produced by all types of C. perfringens (type A and C); classified as a diffusible LECITHINASE that lyses endothelial cells, erythrocytes, platelets, and leukocytes. Also causes increased vascular permeability and tissue destruction.
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Clostridium difficile
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primary cause of antibiotic-associated gastrointestinal disease (ie CLINDAMYCIN, Cephalosporins, Fluoroquinolones)
Chemotherapy can also cause problems! Bloody diarrhea is common along with fever and fatigue causes PSEUDOMEMBRANOUS COLITIS: inflammatory cells, white fibrin, and mucus on colon (looks like Tennis Rackets) |
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2 microorganisms commonly
associated with antibiotic-causing diarrhea |
1) Clostridium difficile
2) Candida albicans: a yeast infections in women caused by broad spectrum antibiotics, use over an extended period of time, and/or multiple antibiotics taken at once |
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Toxin A or Toxin B
Diagnosis of C. difficile |
Both inhibit components of cell signaling pathways by glycosylation (both are always present in C. difficile infection)
Toxin A (an enterotoxin): stimulates the movement of neutrophils to the ileum (cytokine release) and the disruption of cell junctions (diarrhea). Toxin B (a cytotoxin): actin depolymerization and hence CYTOSKELETON DAMAGE . Toxin B is 1000X more potent than Toxin A. TX: Discontinue problematic antibiotic; severe cases may require metronidazole or vancomycin Both detected w/ ELISA |
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Listeria monocytogenes
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important potential pathogen for
PREGNANT WOMEN due to significant increase in SPONTANEOUS ABORTIONS Gram-positive motile rod; intracellular pathogen found in soil, decaying vegetable matter, animal feces, SOFT CHEESE, undercooked meat and poultry, contaminated milk, unwashed raw vegetables Grows well at cold temps (refrigerator), easily killed by heat Not the most common cause of food poisoning, but has the highest mortality rate (20-30%) •mild GI issues, flu-like symptoms; most common cause of MENINGITIS and bacteremia/septicemia •treatment: penicillins commet tail (flagella allows it to evade immune system and get into blood) |
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Vibrio cholerae
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Gram neg, curved rod, single polar flagella
O-Polysaccharide is used for dividing V. cholerae into serogroups (01 and 0139 are the most commonly associated with epidemics); O1 is further divided into the “CLASSIC” and “EL TOR” biotypes From CONTAMINATED WATER or seafood that was living in it. SX: Depends on serogroup and biotype; mild to severe fatal diarrhea, usually a PROFUSE WATER DIARRHEA OR RICE-WATER STOOLS. Low gastric acidity can decrease infectious dose Death rate 50%!!! w/o TX TX: fluid and electrolyte replacement (glucose, salt, and water), Doxycyline |
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Cholera toxin of
Vibrio cholerae |
main virulence factor
Mechanism of Action: B subunit binds to GM1 R promoting uptake of A subunit via endocytosis. A subunit ribosylates the Gαs resulting in a constitutively active adenylate cyclase. The increase in cAMP activates PKA which through phosphorylation of CFTR, promotes water and Cl- loss through the channel |
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Staphylococcus aureus
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Gram-positive, cocci
intoxication (killed by heating but toxin is a heat-stable enterotoxin) Problem foods: processed meats (S. aureus is very salt tolerant), custard filled pastries, potato salad, and ice cream SX: develop rapidly within 4 hours and include diarrhea, vomiting, abdominal pain, and nausea; lasts ~24 hours |
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Bacillus cereus
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Gram-positive spore-forming rod
Emetic form - associated w/ RICE; VOMITING, nausea, abdominal cramps; 8-10 hrs; heat stable Diarrheal form: DIARRHEA, nausea, abdominal cramps; 20-36 hrs; heat labile not serious, clear it and move on w/ life |
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Parasites that cause Diarrhea
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unit 3, week 3 continued
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Cryptosporidium parvum
(Sporozoa) |
M: small round, along brush border
Common in water kids Acid fast stain Very tiny –prevents flocculation Also resistant to chlorine treatment of water Self limiting ~ 10 days Tx: hydrate only (except AIDs pts who need antiprotozoan drugs) |
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Entamoeba histolyticum
(amoeba) |
M: nucleus w/ evenly arranged chromatin on nuclear membrane, sometimes visible ingested RBCs (in pt w/ dysentery)
Carried by Roaches and Flies Could be confused w/ E. dispar (asymptomatic, non-pathogenic, & doesn’t carry RBCs) -> possible non-infectious cause for diarrhea; differentiate via PCR Invasive - can go to liver, brain, colon |
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Giardia lamblia
(Flagellate) |
M: tear dropped shape with smiley face
Daycares Lakes Gastric bypass (have lower stomach acidity) Cysts are the most infectious form |
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Balantidium coli (ciliate)
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M: large bean shaped macronucleus and small micronucleus
Contracted from animals (swine or monkey feces) Bloody pus diarrhea |
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Worms (helminths) causing Diarrhea
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unit 3, week 3 continued
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Strongyloides stercoralis
(Nematode) |
M: short mouth opening and a packet of genital primordial cells, and a notched tail of the filariform (aka Threadworm)
Risk: kids Notes: Filariform is infectious form; Infect via skin contact |
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Trichuris trichiura (Nematode)
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M: eggs are barrel shaped with clear mucoid-appearing polar plugs.
Risk: Kids (affects nutrition, growth, & development), asymptomatic in adults; Human transmission |
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Schistosoma mansoni
(trematode) |
M: eggs are yellow-brown, elongated, void, and have one large lateral spine
Risk: Intermediate host (bw humans): snails Notes: Impact many systems; Round but part of flatworms; Losses tail when it penetrates skin; Eggs cause intestinal discomfort; Can cause itchy skin (Cercarial dermatitis), Lymphadenopathy of liver, Ascites |
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Ascaris lumbricoides
(Nematode) |
M: nubby, fertilized egg is broadly oval with a thick mamillated coat, golden brown. Adults worms are cylindrical with tapering anterior end. Can be 15 to 35 cm long (BIG Adults!)
Risk: Human feces for fertilaztion of veggies/fruits Notes: Pneumonitis (infl of lungs, cough phlem, swallow, infect intestinal tract) |
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Unit 3 Week 4
NO MICRO =) !!!!!!!!!!! |
=) =) =")
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Unit 3 Week 5
Abdominal Pain & GI bleed |
Helicobactor pylori and Campylobacter SPP
Abdominal Discomfort - Flukes and Worms |
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Campylobacter
Epidemiology and Transmission |
• Transmission: Zoonotic
○ Food: Poultry, rRAW MILK, Water ○ C. upsaliensis: puppies ○ C. fetus: cattle & sheep • Common in spring in INFANTS/young KIDS • Milder ds in endemic regions • Prolonged ds in hypogamaglobulinemic • 1/1000 diagnosed infections lead to Guillan-Barre (paralysis) • MOST COMMON BACTERIAL CAUSE OF DIARRHEAL ILLNESS IN US |
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Campylobacter
Diagnosis |
• Microscopy: thin, S-shaped in stool specimen (50-70% sensitive)
• Antigen detection (80-90% sens) • Culture: microaerophilic atmosphere, elevated incubation temp (42 C), selective media w/ blood & charcoal to remove O radicals, antibiotics, slow growing (48-72 hrs) • ID in culture based on growth under selective conditions, typical microscopic morphology, and (+) oxidase & catalase |
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Campylobacter
Treatment |
• Fluid & electrolyte replacement
• Antibiotics for PT w/ high fever, bloody diarrhea, & 8+ stools/day • Use erythromycin (eliminates carriage in 72 hrs), most are resistant to penicillin |
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Campylobacter
Prognosis |
• Most self-limiting or recover w/ antibiotic TX
• Reactive Arthritis or Reiter's syndrome in HLA-B-27 (+) for months • Dearths can occur due to Guillan Barre, dehydration, malnutrition, or in pt w/ cirrhosis, DM, or IMCP |
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C. jejuni
Clinical Presentation |
• Bacterial gastroenteritis: damage to mucosal surfaces of jejunum
• diahhrea, cramping, abdominal pain, & fever • Lasts ~1 wk • Diarrhea can be bloody and accompanied by N/V • Pain can mimic appendicitis • Can spread to bloodstream in immunocompromised (IMCP) Grows at 42C |
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C. fetus
Clinical Presentation |
• Easily spreads from GI to blood: Intravascular and extraintestinal infections
• Endocarditis, septic thrombophlebitis, Bacteremia, arthritis, septic abortion, meningoencephalitis, spontaneous prmary peritonitis • Lethal to fetus • S-protein is heat stable and confers complement resistance Grows at 37C |
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Helicobactor Pylori
Clinical Presentation |
• Most asymptomatic, carriers
• Acute: fullness, N/V; maybe upper abd pain, fever, & hypochlorhydria (decreased acid production); lasts 12 days • Chronic : possibly upper abd pain worse w/ eating, dark stools, indigestion; rarely N/V, anorexia • Atrophic gastritis worse w/ time which predisposes development of gastric cancer • Peptic ulcer ds in 10% infected • Increased risk for gastric cancer (1-3%) & Mucosal lymphoid tissue B-cell lymphomas (MALT <0.1%) |
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Helicobactor Pylori
Colonization/Pathogenesis & Immunity |
• Lives in mucus layer in stomach (mostly Antrum) & sometimes duodenum & esophagus; microaerophilic
• Blocks acid production locally via production of Urease (ammonia) and bacterial acid inhibitory protein • Adherence: HOPs genes, protects against peristalsis & mucosal shedding • Mucinase & Phospholipase • LPS: protection from immune clearance (resembles blood group antigen) • VacA: causes osmotic swelling resulting in cell vacuolation, pore formation, & suppresses immune sys by down regulating B & C cell activity • CagA: changes cell shape/fx, cell cycle events, cytokine production, and induces IL-8 production (inflammation) • PT has increased risk of severe gastritis, peptic ulcer ds, & adenocarcinoma of distal stomach |
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Helicobactor Pylori
Epidemiology and Transmission |
• ~ 1/2 world's population infected
• Patterns of gastritis ○ Individuals w/ gastric carcinoma & gastric ulcers likely had multifocal atrophic gastritis ○ Individuals w/ duodenal ulcer/peptic ulcer likely had antral-predominant gastritis |
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Helicobactor Pylori
Diagnosis |
• Preferred: Urease Breath test (non-invasive; feed pt labeled urea, organism breaks it down into ammonia and co2, co2 is detected for + result)
• Microscopy of biopsy ○ gold standard is histological examination for ID gastritis ○ Warthrin-Starry Silver stain, El-Zimaity triple stain, & rapid urease test for ID of H. pylori bacterium • CLOtest: qualitative assay of biopsy based on detection of urease, produced by H. pylori; turns from yellow to red if positive due to rise in pH • Culture: not practical, takes wks to get result; better f/ biopsy than stool, but invasive |
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Helicobactor Pylori
Concern for older adults - 4 reasons Possible outcomes |
• Concern for older adults:
○ higher incidence of gastric atrophy & atrophic gastritis ○ larger use of NSAIDs, cigarettes, & alcohol ○ Sx of infection masked by comorbidities ○ Significant clarithromycin resistance • Multiple ds outcomes: Gastritis, peptic ulcers (gastric or duodenal), cancer (MALT B-cell lymphoma or gastric cancer) |
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What is Infectious Peritonitis?
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Diffuse inflammation of peritoneus
2 types: Primary & Secondary |
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Primary Peritonitis (Spontaneous)
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Infection in peritoneal cavity w/o any obvious source of contamination
CP: fever, abd pain, n/v, diarrhea, abd tenderness, hypoactive bowel sounds Bact: E. coli (GI source) >Klebsiella pneumoniae, S. pneumonia (lung source), & other streptococcal species; Staph can occur but rarely. Almost always caused by AEROBIC BACTERIA (ascitis doesn’t allow survival of anaerobes). Can cause bacteremia Eiology: usu in PTs w/ cirrhosis & ascites, or kids w/ nephrotic syndrome |
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Secondary Peritonitis
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Caused by spilalge of GI or GU microgs into peritoneal cavity
CP: mod->severe abd pain where any motion aggravates pain; fever, progression to sepsis or septic shock Bact: depends on site of perforation along GI (gram+ ogs predominate in upper GI while gram- in lower GI) - Stomach: facultative gram+, salivary mirogs ie Candida, lactobacilli, & strep (usu realtively bact free b/c of high acidity) - Colon E. coli (most freq isolated facultative anaerobe) B. fragilis (most freq isolated obligate anaerobe) - Appendicitis: mostly anaerobes, mostly Prevotella melaninogenica Etio: perforation of a peptic ulcer; traumatic perforation of uterus, bladder, stomach, or sml/lg int, PID, appendicitis, diverticulitis, etc |
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Management of Peritonitis
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• Triple therapy w/ ampicillin (for enterococci), genatamicin (for aerobic gram- rods), & metronidazole (for anaerobes)
• Surgery to correct perforation, leaks, or abscesses • Lavage (washing out) to cleanse abdomen |
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What are Nematodes?
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Worms
Large in size, cylindrical unsegmented bodies “round worms” Incl Ascaris lumbricoides, Taxacara canis, Trichuris trichiura |
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Ascaris lumbricoides
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Description: nubby eggs, Big Adult worms
Risk: Human feces for fertilaztion of veggies/fruits Notes: Pneumonitis (infl of lungs, cough phlem, swallow, infect intestinal tract) Symptoms Pneumonitis, vague intestinal complaints or asymptomatic |
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Toxocara canis
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Description: Eggs resemble ascaris eggs except for the mamillated coat
Acquired by consumption of contaminated soil. Animal reservoirs: Dogs and Cats. Human is dead end host Syndromes/ Symptoms Depends on the number of migrating larvae. Ranging from asymptomatic to severe disease. VLM, OLM, NLM. VLM: fever hepatomegaly, hyperglobulinemia, pulmonary infiltrates, cough, neurological disturbances and endophthalmitis |
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Trichuris trichiura
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Description: barrel shaped eggs w/ clear mucoid-appearing POLAR PLUG
Risk: Kids (affects nutrition, growth, & development), asymptomatic in adults Human transmission Clinical Specimen Eggs in the Stool. It is very unusual to see adult worms as they are attached to the intestinal wall Symptoms Abdominal cramps, distention, bloody diarrhea, rectal prolapse ( children), weakness and weight loss. |
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What are Trematodes?
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Flat, fleshy leaf shaped worms, w/2 muscular suckers, most hermaphroditic (except schistosomes), req intermediate hosts, operculum (except schistosomes)
Incl: Fasciolopsis buski, Fasciola Hepatica, Opisthorchis sinensis |
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Fasciolopsis buski
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Animal reservoirs: Pigs, dogs and rabbits SNAIL
Eating infective metacercariae on raw aquatic vegetation particularly WATER CHESTNUTS Symptoms Intestinal inflammation, duodenal ulceration and hemorrhage |
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Fasciola Hepatica
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Animal Reservoir: Sheep/Herbivores
Acquired by eating contaminated WATER CRESS contaminated with the Metacercariae Symptoms Liver irritation tenderness, hepatomegaly. URQ pain, Hepatitis, hyperplasia, biliary obstruction, liver rot, portal cirrhosis |
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Opisthorchis sinensis
( Clonorchis sinensis) Aka Chinese River Fluke |
Animal reservoir: Fish
Acquired by eating raw or poorly cooked fresh water fish Symptoms Epigastric pain, hepatomegaly, biliary obstruction, cholecystitis, cholelithiasis, pancreatitis liver abscess Epidemiology: EAST ASIA |
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What are Cestodes?
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Tape worms, Flat and ribbon like, head (Scolex) equipped with organs of attachment, hermaphroditic, eggs Not operculated & contain 6 hooked hexacanth embryo
Incl: Taenia solium, Echinococcus granulosus |
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Taenia solium
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Acquired
Adult worm obtained by ingestion of infective cysts (cysticerci) from infected PORK Also BEAR Symptoms Adult worm can cause abdominal discomfort and chronic indigestion and diarrhea Sxs depends on worm load (how many worms are there) Body site(s) Intestine Epidemiology WORLDWIDE, primarily human to human transmission |
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Echinococcus granulosus
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Animal reservoir: DOGS and Herbivores/SHEEP requires intermediate and definitive host.
Humans (eat herbivore tissue) are the dead-end host. Ingestion of eggs from the tape worm in the dog’s intestine Symptoms In the liver, the HYDATID CYSTS may exert pressure on both bile ducts and blood vessels and create pain and biliary rupture. Most hydatid cysts reside in the liver causing symptoms including CHRONIC ABDOMINAL DISCOMFORT W/ OCCASIONAL PALPABLE MASS Body site(s) Hydatid cysts in liver, lungs and other tissues Epi: WORLD-WIDE |
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U3 W9
Abnormal WBCs & Lymphadenopathy |
HIV-AIDs
Infectious Lymphadenopathy |
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U3 W10
Abnormal Coagulation |
Infection and Bleeding/Clotting
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Clinical Features of Viral Hemorrhagic Fever Syndrome?
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Fever, myalgia, & malase that lasts 3-4 days
Progression: Rash (only some), prostration, evidence of cap leaking, hemorrhage (only 50%), CNS depression, & shock |
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Ribavirin
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Ribavirin:
antiviral medication that interferes w/ RNA metabolism required for viral metabolism (used for Lassa, Argentine HF, CCHF; NOT used for Filoviruses, Rift Valley) |
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Arenaviridae Family
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enveloped, spherical particles w/ a 2 segment AMBISENSE RNA genome; helical nucleocapsid
Family is associated w. chronic infections of rodents; prevent by rodent control Incl: Lassa Fever |
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Lassa Fever
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Lassa fever - W Africa & parts of Asia; fever, facial swelling, abcominal pain; severe infection associated w/ hearing loss, tremors, & bleeding
Virus has sandy appearance due to presence of ribosomes |
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Bunyaviridae
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spherical, enveloped, w/ spikes projecting f/ surface of virions; 3 segment (+) RNA (L, M, S)
Incl: La Crosse virus, Crimean congo, Rift Valley Fever, & Hantaan Virus |
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La Crosse Virus
Bunyaviridae Bunyavirus |
LaCrosse viruse
Epi: N CENTRAL & EASTERN US; tree hole breeding Vector: Aedes Triseriatus mosquito propagated by sml animals ie CHIPMUNKS causes MENINGITIS & ENCEPHALITIS - acute CNS ds in KIDS |
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Crimean Congo
Bunyaviridae Nairovirus |
Epi: Old world (SubSaharan Africa, Middle East, China, India, but mainly Africa)
Vector: Ixodid tick -> Ostrich CP: Initial: red eyes, flushed face, petechiae, jaundice Advanced: ecchymosis, bleeding, DISSEMINATED INTRAVASCULAR COAGULATION (DIC), severe thrombocytopenia COMMON |
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Rift Valley Fever
Bunyavirida Phlebovirus |
SubSaharan Africa
Vector: Mosquito borne (Aedes mcintoshi) water breeding (EPIDEMIC DURING HEAVY RAINFALL) -> sheep & cattle; No interhuman transmission CP: usu asymp or mod illness; 1% mortality |
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Hantaan virus
Bunyavirida Hantavirus |
Epi:
N AMERICA -> Sin Nombre Virus ASIA -> HFRS CP: fever, shock, pulmonary edema, SUNBURN FLUSH |
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FILOviridae Family
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long, filamentous, enveloped pleomorphic viruses
cause severe hemorrhagic fever, characterized by widespread bleeding into skin, mucous membranes, visceral organs, & GI tract; high mortality rate of >50% Incl Marburg & Ebola |
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Marburg
Where do you see it most? What's the vector that carries it? |
Epi: EUROPE (GERMANY)
Vector: African Green Monkeys |
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Ebola
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Epi: Zaire (Ivory Coast) & Sudan (S Africa)
Vector: Fruit bats Virus looks like it has a knot on one end |
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Ebola Pathogenesis
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Virus spreads f/ infection site to regional LN, liver, & spleen
Doesn't infect lymphocytes - just APOPTOSIS Results in release of soluble factors (ie NO) f/ monocytes & macs -> vascular impariment & leakage -> hypotension -> shock & multiorgan failure |
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FLAVIviridae
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enveloped, (+) ssRNA
Incl Dengue & Yellow Fever Vector for Dengue & Yellow fever is the Aegytpti mosquito |
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Dengue Fever
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Dengue Fever - SE ASIA
Sx: sudden onset of fever (BONE-BREAK FEVER), HA, & sever myalgia; severe cases may lead to shock, hemorrhage, & death |
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Yellow Fever
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Yellow fever - tropical regions of S AMERICA & Africa
Sx: fever, HA, chills, N/V, & occasionally jaundice; serious cases can affect liver & kidneys Prevent w/ live attenuated, highly effective, safe vaccine |
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Emerging Virus
What is it and what are the 5 mechs f/ which they can originate? |
Emerging virus- viruses that only recently have become apparent
1. When technology becomes sufficiently advanced to allow detection 2. When humans change their lifestyles- increased concentration of people (Measles), better personal and public hygiene (Polio), increased urbanization, travel for work, prostitution (HIV) 3. When humans “turn over rocks”- new exposure to virus upon clearing rainforests or pop of new environments (Ebola, Marburg, West Nile) 4. Natural changes in the environment (Hanta virus) 5. When viruses mutate or reassert their genome (HIV, HCV, swine flu) |
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Rickettsia genus
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Tickborne, intracellular bacterial parasite that uses bacterial OmpA for adherence to endothelial cells
Pathogenesis: bacteria penetrate cell by endocytosis and are released into cytoplasm to replicate primary clinical manifestation (rash and ecchymoses) tend to occur because of replication of the bacteria in endothelial cells with subsequent damage to cells and leakage of blood vessels Incl Rocky Mt Spotted Fever |
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Rocky Mountain spotted Fever
Symptoms? |
High fever, headache, malaise, myalgias, nausea, vomiting, abdominal pain and diarrhea; after 3 days a rash appears on wrist, hands and feet (soles and palms) and spreads to trunk; hypovolemia, hypoproteinemia
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U3W6
Liver Fx Tests & Jaundice |
Liver Infections
Viral Hepatitis |
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Liver Infections - most common organism
Amebic Liver Abscess |
Entamoeba histolytica or Entamoeba dispar
Worldwide primarily human to human but rare now in US due to better sanitation. |
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Liver Infections - most common organism
Pyogenic Liver Abscess Gram Negatives (2) |
Escherichia coli
Klebsiella spp |
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Liver Infections - most common organism
Pyogenic Liver Abscess GRAM POSITIVES (3) |
Streptococcus intermedius
Enterococci Viridans Streptococci |
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Liver Infections - most common organism
Pyogenic Liver Abscess ANAEROBE (1) |
Bacteroides
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Liver Infections - most common organism
Liver Abscess in people with hemachromatosis (1) |
Gram negative (Enterobacteraceae)
Yersinia enterocolitica more common in European countries and colder regions of the US |
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Liver Infections - most common organism
Biliary System infections: Acute Cholecystis and Acute Cholangitis Gram negatives (3) |
Escherichia coli
Klebsiella spp, & Enterobacter spp very common in US |
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Liver Infections - most common organism
Biliary System infections: Acute Cholecystis and Acute Cholangitis Gram positive (1) |
Enterococci
very common in US |
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Liver Infections - most common organism
Biliary System infections: Acute Cholecystis and Acute Cholangitis Anaerobes (3) |
Bacteroides spp F
usobacterium spp and Clostridia very common in US |
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Liver Infections - most common organism
Biliary Obstruction and chronic infection can lead to adenocarcinoma of the bile ducts (1) |
Trematode-Chinese liver fluke
Opisthorchis (Clonorchis) sinensis Undercooked fish; China , Japan, Korea, Vietnam. |
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Liver Infections - Most common organisms
Hepatitis, hyperplasia, Biliary obstruction (1) |
Trematode-Sheep liver fluke
Fasciola hepatica Cattle, goats, sheep/ eating WATERCRESS. Rare in US. Found in Bolivia, Ecuador, Egypt, France Iran, Peru and Portugal |
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Liver Infections - Most common organisms
Schistosomiasis, Bilharziasis, Snail fever, Clay pipestem fibrosis |
Trematode –liver fluke
Schistosoma mansoni Western and central Africa, Egypt, Malagasy, Arabian peninsula, Brazil, Suriname, Venezuela, West Indies. |
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Liver Infections - Most common organisms
Hydatid cysts in liver or lung |
Cestode- tape worms
Echinococcus granulosus Associated with SHEEP raising World Wide especially in Europe, S. America, Africa, Asia, Australia and New Zealand |
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Liver Infections - Most common organisms
Alveolar hydatid cyst disease |
Cestode- tape worms
Echinococcus multilocularis FOXES and WOLVES in Norther areas such as Canada, Soviet Union, H. Japan, Cent Europe, Alaska, Montana, N.& s Dakota, Minnesota and Iowa |
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Liver Infections - Most common organisms
Biliary obstruction (1) |
Nematode
Ascaris lumbricoides World wide |
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Liver Infections - Most common organisms
AIDS-Related Sclerosing cholangitis Protozoan (2) |
Cryptosporidium hominis
Cryptosporidium parvum World wide |
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Liver Infections - Most common organisms
AIDS-Related Sclerosing cholangitis Herpesvirus (1) |
Cytomegalovirus
World wide |
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Liver Infections - Most common organisms
Yellow Fever |
Flavivirus
Yellow Fever virus Aedes aegypti mosquito vector; Africa and South America |
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U3 W7&8
Abnormal Hemoglobin |
Infection and Anemia
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Plasmodium species
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human infection via Anopheles mosquito, introducing SPOROZOITES via it's SALIVA into circulatory sys
Sporozoites carried to LIVER, where SCHIZOGANY occurs (ring -> trophozoite->schizont) RBC rupter releases MEROZOITES |
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Plasmodium vivax
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Benign tertian (fever/chills every 3rd day)
invades only young rbcs see enlarged rbcs w/ Schuffner dots (pink granules); Trophozoite-ring shapped, contain 24 merozoites most prevalent in humans Most survive for yrs w/o tx. left untx can lead to brain, kidney, & liver damage due to plugging by masses of adherent rbcs |
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P. ovale
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Benign tertian
schizonts contain 12 merozoites; Fimbriation & Schuffer dots tripical africa, asia, S america untx inf last only 1 yr |
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P. malariae
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Quartan (fever patterns every 4th days)
infect only mature rbcs - no enlargment trophozoite band form; Schizont contain 8 merozoite Rosette; Ziemann dots (reddish ganules) untx inf may last 20 yrs |
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P. falciparum
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malignant tertian
Single RBC may contain 3-4 merozoite rings; Aplique; Crescentic gametocytes; Maurer dots (reddish granules) common co-infection w/ HIV tropicla and subtropical regions Mostly fatal Kidney damage - Blackwater Fever often in combo w/ P. vivax |
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Bebesia species
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mrophologically resembles plasmodia; most asymptomatic
infection transmitted by Ixodid ticks Bebesia microti is usual cause of babesiosis in US Tx w/ antiprotozoal drugs |
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Ancylostoma duodenale & Necator americanus
hookworms |
cause MICROCYTIC HYPOCHROMIC ANEMIA
filariform larvae (worm) = infectious form, penetrates skin of feet |
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Diphyllobothrium latum
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causes MEGALOBLASTIC ANEMIA
Mediates dissociation of vit B12- intrinsic factor complex in lumen and uses it itself Vit B12 deficiency -> impaired DNA synthesis, salt craving, intermitten abdominal pain carried by freshwater fish parasite - tapeworm (cestodes) |
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Bartonella bacilliformis
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Gram neg Rod
transmission via SANDFLY bite Grows well at LOWER temps - ANDES mts causes HEMOLYTIC ANEMIA Carion ds - actue febrile illness; Oroya fever - severe anemia, lethal; Verruga peruana - blood filled nodules |
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Parvovirus B19
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Non-Env, Icosahedral, DNA virus that forms Hairpin loops on itself
Acute Infection: Child gets Fifth Ds (slapped cheek) Adult gets Polyarthropathy PT w/ Chronic Hemolytic Anemia get Transient Aplastic Crisis (can aslo get PPGSS which is gloves & socks syndrome of rash, aka B12 dermatosis) Chronic Infection Immunocompromised get Pure Red Cell Aplasia Fetus gets Congenital anemia or worse Hydrops fetalis (accumulation of fluid in baby, severe) |
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Infections that cause Aplastic Anemia (5 viruses)
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Hepatitis virus, CMV, EBV, HSV and B19
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Infections that cause Hemolytic anemia or iron deficiency anemia (2 parasites)
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Bebesia leading to cell lysis
invasion of reticuloendothelial system by Leishmania (blood parasite) causes prod of oxidative metabolic products (oxidative stress) that lyse RBCs |
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Infections that cuase Autoimmune Hemolytic Anemia (3 viruses)
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EBV, CMV, HIV infecitons
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