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147 Cards in this Set

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Nausea and Vomiting
wk 21
Unit 3, week 2
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
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
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
Adenovirus
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)
Adenovirus Interference w/ Host defense (3 ways)
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
Norovirus (Norwalk)
Naked capsid
(+) ss RNA

Low infectious dose, Foodborne - contaminated food ie shellfish
ADULT gastroenteritis
Star morphology

Caliciviridae family
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
Calicivirus
Naked Capsid, (+)ssRNA
Single protein capsid
M: cup-shaped indentions
Calciviridae family
Astrovirus
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
Enterobacteriaceae
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
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.
Salmonella
non-typhoid
Host: broad range (turtle)
Sxs: Gastroenteritis, abdominal pain, vomiting, and inflammatory diarrhrea
Salmonella Virulence Factors
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.
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)
Shigella dysenteriae
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
Shigella sonnei
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)
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.
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.
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.
Enterotoxigenic E. coli (ETEC)
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.
Enterhemorrhagic E. coli (EHEC)
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
Enteroinvasive E. coli (EIEC)
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
Entero-aggregative E. coli(EAEC)
children as watery diarrhea, vomiting, dehydration and sometimes a UTI.
Entero-pathogenic E. coli (EPEC)
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.
Sorbitol-MacConkey Media (SMAC)
no lactose

E. coli 0157:H7; no fermentation of sorbitol on SMAC media


A non-0157:H7 strain; fermentation of sorbitol on SMAC media
Hemolytic Uremic Syndrome (HUS)
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.
Yersinia enterocolitica
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
Enterobacteriaceae
all glucose fermenters and do not produce cytochrome c oxidase
E. coli
(lab)
Lactose (+)
Indole (+)
Citrase (-)
Citrobacter
(lab)
Lactose (+)
Urease (+)
H2S (+)
Klebsiella
(lab)
Lactose (+)
Urease (+)
H2S (-)
Enterobacter
(lab)
Lactose (+)
Urease (-)
Proteus
(lab)
Lactose (-)
Glucose (+)
Motile
Urease (+)

(catheters)
Salmonella
(lab)
Lactose (-)
Glucose (+)
Motile
Urease (-)
H2S (+)
Serratia
(lab)
Lactose (-)
Glucose (+)
Motile
Urease (-)
H2S (-)

pink on TSA
Shigella
(lab)
Lactose (-)
Glucose (+)
Non - Motile
H2S (-)
Pseudomonas
(lab)
Lactose (-)
Glucose (-)
Oxidase (+)
Diarrhea
wk 22
Unit 3, week 3
Food poisoning
microorganism is ingested
Food intoxication
Food contaminated with a toxin
Symptoms appear sooner than those of a food poisoning.
Campylobacter jejuni
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
Clostridium: C. botulinum, C. perfringens, and C. difficile
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
Foodborne botulism
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
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
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
Clostridium perfringens
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.
Alpha Toxin
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.
Clostridium difficile
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)
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
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
Listeria monocytogenes
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)
Vibrio cholerae
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
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
Staphylococcus aureus
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
Bacillus cereus
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
Parasites that cause Diarrhea
unit 3, week 3 continued
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)
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
Giardia lamblia

(Flagellate)
M: tear dropped shape with smiley face

Daycares
Lakes
Gastric bypass (have lower stomach acidity)

Cysts are the most infectious form
Balantidium coli (ciliate)
M: large bean shaped macronucleus and small micronucleus

Contracted from animals (swine or monkey feces)

Bloody pus diarrhea
Worms (helminths) causing Diarrhea
unit 3, week 3 continued
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
Trichuris trichiura (Nematode)
M: eggs are barrel shaped with clear mucoid-appearing polar plugs.

Risk: Kids (affects nutrition, growth, & development), asymptomatic in adults; Human transmission
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
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)
Unit 3 Week 4
NO MICRO =) !!!!!!!!!!!
=) =) =")
Unit 3 Week 5
Abdominal Pain & GI bleed
Helicobactor pylori and Campylobacter SPP

Abdominal Discomfort - Flukes and Worms
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
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
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
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
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
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
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%)
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
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
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
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)
What is Infectious Peritonitis?
Diffuse inflammation of peritoneus

2 types: Primary & Secondary
Primary Peritonitis (Spontaneous)
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
Secondary Peritonitis
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
Management of Peritonitis
• 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
What are Nematodes?
Worms
Large in size, cylindrical unsegmented bodies “round worms”

Incl Ascaris lumbricoides, Taxacara canis, Trichuris trichiura
Ascaris lumbricoides
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
Toxocara canis
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
Trichuris trichiura
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.
What are Trematodes?
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
Fasciolopsis buski
Animal reservoirs: Pigs, dogs and rabbits SNAIL
Eating infective metacercariae on raw aquatic vegetation particularly WATER CHESTNUTS

Symptoms
Intestinal inflammation, duodenal ulceration and hemorrhage
Fasciola Hepatica
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
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
What are Cestodes?
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
Taenia solium
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
Echinococcus granulosus
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
U3 W9
Abnormal WBCs & Lymphadenopathy
HIV-AIDs

Infectious Lymphadenopathy
U3 W10
Abnormal Coagulation
Infection and Bleeding/Clotting
Clinical Features of Viral Hemorrhagic Fever Syndrome?
Fever, myalgia, & malase that lasts 3-4 days

Progression: Rash (only some), prostration, evidence of cap leaking, hemorrhage (only 50%), CNS depression, & shock
Ribavirin
Ribavirin:
antiviral medication that interferes w/ RNA metabolism required for viral metabolism (used for Lassa, Argentine HF, CCHF; NOT used for Filoviruses, Rift Valley)
Arenaviridae Family
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
Lassa Fever
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
Bunyaviridae
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
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
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
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
Hantaan virus

Bunyavirida Hantavirus
Epi:
N AMERICA -> Sin Nombre Virus
ASIA -> HFRS
CP: fever, shock, pulmonary edema, SUNBURN FLUSH
FILOviridae Family
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
Marburg

Where do you see it most?
What's the vector that carries it?
Epi: EUROPE (GERMANY)

Vector: African Green Monkeys
Ebola
Epi: Zaire (Ivory Coast) & Sudan (S Africa)

Vector: Fruit bats

Virus looks like it has a knot on one end
Ebola Pathogenesis
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
FLAVIviridae
enveloped, (+) ssRNA

Incl Dengue & Yellow Fever

Vector for Dengue & Yellow fever is the Aegytpti mosquito
Dengue Fever
Dengue Fever - SE ASIA

Sx: sudden onset of fever (BONE-BREAK FEVER), HA, & sever myalgia; severe cases may lead to shock, hemorrhage, & death
Yellow Fever
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
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)
Rickettsia genus
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
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
U3W6
Liver Fx Tests & Jaundice
Liver Infections

Viral Hepatitis
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.
Liver Infections - most common organism

Pyogenic Liver Abscess
Gram Negatives (2)
Escherichia coli
Klebsiella spp
Liver Infections - most common organism

Pyogenic Liver Abscess
GRAM POSITIVES (3)
Streptococcus intermedius
Enterococci
Viridans Streptococci
Liver Infections - most common organism

Pyogenic Liver Abscess
ANAEROBE (1)
Bacteroides
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
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
Liver Infections - most common organism

Biliary System infections: Acute Cholecystis and Acute Cholangitis

Gram positive (1)
Enterococci

very common in US
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
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.
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
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.
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
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
Liver Infections - Most common organisms

Biliary obstruction (1)
Nematode
Ascaris lumbricoides
World wide
Liver Infections - Most common organisms

AIDS-Related Sclerosing cholangitis

Protozoan (2)
Cryptosporidium hominis
Cryptosporidium parvum

World wide
Liver Infections - Most common organisms

AIDS-Related Sclerosing cholangitis

Herpesvirus (1)
Cytomegalovirus
World wide
Liver Infections - Most common organisms

Yellow Fever
Flavivirus

Yellow Fever virus

Aedes aegypti mosquito vector; Africa and South America
U3 W7&8
Abnormal Hemoglobin
Infection and Anemia
Plasmodium species
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
Plasmodium vivax
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
P. ovale
Benign tertian

schizonts contain 12 merozoites;
Fimbriation & Schuffer dots

tripical africa, asia, S america

untx inf last only 1 yr
P. malariae
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
P. falciparum
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
Bebesia species
mrophologically resembles plasmodia; most asymptomatic

infection transmitted by Ixodid ticks

Bebesia microti is usual cause of babesiosis in US

Tx w/ antiprotozoal drugs
Ancylostoma duodenale & Necator americanus

hookworms
cause MICROCYTIC HYPOCHROMIC ANEMIA

filariform larvae (worm) = infectious form, penetrates skin of feet
Diphyllobothrium latum
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)
Bartonella bacilliformis
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
Parvovirus B19
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)
Infections that cause Aplastic Anemia (5 viruses)
Hepatitis virus, CMV, EBV, HSV and B19
Infections that cause Hemolytic anemia or iron deficiency anemia (2 parasites)
Bebesia leading to cell lysis

invasion of reticuloendothelial system by Leishmania (blood parasite) causes prod of oxidative metabolic products (oxidative stress) that lyse RBCs
Infections that cuase Autoimmune Hemolytic Anemia (3 viruses)
EBV, CMV, HIV infecitons