GI bugs Flashcards
what are the adaptive immune response in the GI tract?
dominated by IgA generation. Peyer patches- collections of lymphoid tissue, where M cells (microfold) sample antigen in the lumen, generating endosomes to surround and transport that antigen through the cell, to then release that antigen into the interstitium. There, dendritic cells will phagocytose and subsequently present that antigen to the gut-associated lymphoid tissue (GALT) or to the local mesenteric lymph nodes.
What is the innate immune respnose to the GI tract?
normal flora crowd out pathogens, saliva contains lysozymes “animals licking wounds”
esophagus- can be infected w/ candida in HIV
helicobactor pylori-avoids acid pH minimizing normal flora
peristalsis- important for getting rid of worms in the GI tract
bile- protected detergent in order to break up lipids and envelopes (diarrhea from unenveloped viruses)
peyers patch spots of organized opportunities for lymphacytic engagement w/ flora function of antigen sampling
A syndrome characterized by gastrointestinal symptoms including nausea, vomiting, diarrhea and abdominal discomfort.
Gastroenteritis
ex. stomach flu
Abnormal fecal discharge characterized by frequent and/or fluid stool; usually resulting from disease of the ____ and involving increased fluid and electrolyte loss
what is it where is it located?
Diarrhea
small intestine
Inflammation involving the mucosa of both the small and large intestine
what is it?
give example
Enterocolitis
ex. from typhoid
An inflammatory disorder of the gastrointestinal tract often associated with blood and pus in the feces and accompanied by symptoms of pain, fever, abdominal cramps; usually resulting from disease of the ____
what is it and where is it
Dysentery
large intestine
What are the strategies that a bug can do in order to pathogenize the GI?
Pharmacologic action of bacterial toxins, local or distant to site of infection, e.g. cholera, staphylococcal food poisoning
Local inflammation in response to superficial microbial invasion, e.g. shigellosis, amebiasis
Deep invasion to blood or lymphatics; dissemination to other body sites, dysentery in the large intestine e.g. hepatitis A, enteric fevers
Perforation of mucosal epithelium after infection, surgery or accidental trauma, e.g. peritonitis, intra-abdominal abscesses.
Infection of the gastrointestinal tract can cause damage locally or at distant sites.
describe these organisms commonly found in the GI and if they were found in the animal reservoir, food-brone, or water borne
Campylobacter- chicken, sinniameats most are human to human
Salmonella, campylobacter food supply
Chloerain the water supply
watery diarrhea-suggestive of small intestine
bloddy- tissue penetration, mucosal involvement suggest large intestine
What are the incubation periods of these bugs?
what are the responses of these bugs?
diarrhea, vomiting, abdominal cramps, fever
what do the different factors mean?
multi-days must need to multiply
minutes-hours suggest toxin preformed and triggering an elaborate gut response
multi-week duration suggest attachment and not able to be flushed out
salmonella, campylobactera all go systemic
what are the most common diarrheal disease proportion of children in the world?
A)These GI pathogens are common
B)The diseases they generate have overlapping clinical features
●
Rotavirus- not common in country due to vaccinationrate
Cryptosporidium- attacks immune compromise underreported with mild watery diarrhea for those w/ intact immune systems
patient has watery stools w/ vomiting w/ fever what are the bugs?
watery-small intestine
vomiting- stimulating peristalsis
fever- active inflammation at the gut or going systemic. The presence of fever, which would imply tissue penetration and additional system involvement.
salmonella- PMNs in the stools ex. daycare, pets
vibrio-shellfish
norovirus- nursing homes many strains and can develop new strains
rotavirus- child, usually adults vacccinated
dont need to know EPEC
patient has watery stools w/ vomiting w/ no fever what are the bugs?
The non-fever diarrheas here would involve toxins.
mostly gram +, two gram- very watery- large volume of water of cholera
bloody stool with vomiting w/ no fever or no fever what are the bugs?
EHEC- washington county fair infection
dont worry about first ecoli.
bloody stool w/ vomiting w/ fever
w/out fever
Bloody stoolsare associated with dysenteryand colonic involvement. enterocolitis type of level
PMN in stool means that enough dilation and breakdown to get it from the blood stream
shigella- straight dysentery picture, large intestinal dysentery
camplyobacter contaminated meats and person to person, much more systemic
C. diff.- toxins causing pseudomembrane
fever w/ no neutrophils- battle fought in different territory yersinia- peyer patches and inflammatory disease simmilar to appendicitis presentation
no fever- parasitic not bacterial requring eosinophils ex.entomeobea munching where they end up go into intestinal wall and portal circulation, can create liver abscesses causing right upper quadrant pain
Toxin: works similar to the cholera toxin to activate adenylyl cyclase to elevate cAMPlevels, to keep the chloride CFTRchannels open in the crypt enterocytes, and hence to trigger a watery diarrhea.
Symptoms: bloody diarrhea, hemolytic uremic syndrome.
Certain strains: These contain Shiga toxins with an A:B5 format, where once internalized after one of the five binding units is taken in, the active unit is split and one component acts as an enzyme to then shut down ribosomal function. The appearance of schistocytesin the peripheral smear and inflammation affecting glomeruli and other vessels indicates the presence of endothelial damage and triggering of a microangiopathichemolytic anemia. Dialysis may be necessary as part of the supportive treatment.
requires supportive care, no antibiotics (if antibiotics quinolone for one strain)
what is it?
what is the pathogen category? normal colonic flora? virulence factors? clinical? immune response? treatment and/or prevention? describe how it works in general and the particular strains that cause damage
TheEnterobacteriaceaeare a family of Gram-negative rods well-represented among pathogenic flora, including Escherichia, Salmonella, and others, often with many strains with different pathogenic features. As an example, two major strains of Escherichia coli are enterotoxigenicand enterohemorrhagicE. coli.
Escherichia coli
Pathogen category: G-rod, aerobic, extracellular
Source: normal colonic flora
Virulence factors: capsule, flagellae, pili
Clinical: UTIs, bacteremia from nosocomial exposure, neonatal meningitis
Immune response: Igsto surface features, neutrophils
Treatment and/or prevention:depends on local resistance patterns; oral quinolone
EnterotoxogenicE. coli(ETEC): traveler’s diarrhea. The ETEC toxin works similar to the cholera toxin to activate adenylyl cyclase to elevate cAMPlevels, to keep the chloride CFTRchannels open in the crypt enterocytes, and hence to trigger a watery diarrhea. would treat w/ quinolone
Enterohemorrhagic E. coli (EHEC): the infamous O157:H7strain and others, with bloody diarrhea and risk of hemolytic uremic syndrome. These contain Shiga toxins (commonly due to meat recall) with an A:B5 format, where once internalized after one of the five binding units is taken in, the active unit is split and one component acts as an enzyme to then shut down ribosomal function. The appearance of schistocytesin the peripheral smear and inflammation affecting glomeruli and other vessels indicates the presence of endothelial damage and triggering of a microangiopathichemolytic anemia, sticking up from platelet clumps and act to cut up RBCs or shystocytes. triggering fibrin conduction. very impacting in the kidney hemolytic niuremic syndrome. dont treat w/ antibiotics because you dont want the bacteria to burst more. Dialysis may be necessary as part of the supportive treatment.
Generally speaking, E. coli-induced diarrheas require supportive treatment, not antibiotics. With EHEC, antibiotic treatment may lead to more release of the toxin asthe bacteria die in a lytic fashion.
acute but typically self-limited diarrhea with vomiting; antibiotics are not helpful in mild cases; fluoroquinolones if severe, with azithromycin as second line. gram - rod.
- motile and pathogenic with capsule
- sensitive to stomach acid, hence requiring a large number of ingested bacteria to cause infection
this develops into rose spots ,inflammation, diarrhea (blood, urine, feces)
what is it?
what is the pathogen category? normal colonic flora? virulence factors? clinical? immune response? treatment and/or prevention? describe how it works in general and the particular strains that cause damage
Salmonellaenterica(many serotypes)
Pathogen category: G-rod, aerobic, intracellular
Source: zoonotic transmission; contaminated food products
Virulence factors: antigenic variation, capsule (escapes peyers patch by this), bacterial-mediatedendocytosis
Clinical: salmonellosis, typically gastritis,but can be systemic and typhoidal
Immune response: stomach acidpreventative, neutrophils generate an inflammatory response, T cell-mediated immunity for clearance, Igs
Treatment and/or prevention:typhoidvaccine (not fully effective); ciprofloxacin for gastroenteritis if needed
Salmonellaentericaconsists of many serotypeswell, with a major distinction between typhoid and others. General features of interest include: enters via endocytosis taken up by peyers patch if not caught there can circulate around and cause typhoid fever.
- Gram negative rod, member of the Enterobacteriaceae
- motile and pathogenic with capsule
- sensitive to stomach acid, hence requiring a large number of ingested bacteria to cause infection
- acute but typically self-limited diarrhea with vomiting; antibiotics are not helpful in mild cases; fluoroquinolones if severe, with azithromycin as second line (Sanford Guide).
typhoid fever:
Salmonella enterica subtype typhi: the serotype responsible for typhoid feveris taken up by macrophages to spread throughout the body, with significant systemic signs and symptoms. There are only human carriers for S.typhi, which is particularly associated with gallbladder carriage, e.g., Mary Mallon- cook in 20th century.
Local inflammation and maculopapularrose spots(that represent bacterial embolization) may appear in 50% of typhoid patients as part of that systemicspread.
Typhoid is treatable with ciprofloxacin (except if Asia-acquired, in which caseceftriaxone, azithromycin or chloramphenicol are options. Available vaccines do not give full protection.
transmural infection or inflammation occuring in the mucosa, submucosa, and other layers of the guts hemorrhaging.
rose spots- embolization of the infetion creating spots on the body
invasion of the galbladder- having bacterial shed from the gut not a lot of white cells and can be sanctuary reservoir. common in places w/ bad sanitation due to sheeting of fecal stage
disease with fever and headache prodrome, followed by cramping and bloody diarrhea. gram - rod poultry and beef reservoir
illness can be associated with Guillain-Barrésyndrome, with ganglioside-like components of its LPS triggering autoantibodies against myelin. gram - rod poultry and beef reservoir
what is it?
what is the pathogen category? normal colonic flora? virulence factors? clinical? immune response? treatment and/or prevention? describe how it works in general and the particular strains that cause damage
Campylobacter jejuni
Pathogen category: G-curved rod, microaerophilic, extracellular
Source: zoonotic transmission; contaminated food products
Virulence factors: antigenic variation and motility with flagella
Clinical: dysentery; post infection reactive arthritis, Guillain-Barrésyndrome
Immune response: inflammatory response, Igsand cell-mediated immunity subsequent to infection
Treatment and/or prevention:azithromycin
Campylobacter jejuniis another common cause of inflammatory diarrhea/dysentery. Features of interest:
- Gram-negative curved rod (“gull-wing” pattern), microaerophilic-low O2 environment, treatable with macrolides, truncated villi triggering inflammatory environemnt in the small intestine getting bloody and watery diarrhea to dysentery.
- poultry and beef reservoirs
- disease with fever and headache prodrome, followed by cramping and bloody diarrhea (note the intestinal invasion in the image)
- illness can be associated with Guillain-Barrésyndrome, (percentage of people w/ this conditoin have some kind of infection due to cross reaction) with ganglioside-like components of its LPS triggering autoantibodies against myelin
a patient ate not fully cooked seafood. after several hours to days they developed watery and tinge of blood diarrhea painless watery diarrhea with some fever
another similar strain a patient ingests freshwater producing painlesss watery diarrhea can lead to death from dehydration
what is it?
what is the pathogen category? normal colonic flora? virulence factors? clinical? immune response? treatment and/or prevention? describe how it works in general and the particular strains that cause damage
Vibrio parahaemolyticus
Pathogen category: G-curved rod, aerobic, extracellular
Source: free-livingin salt water
Virulence factors: abilityto penetrate into intestinal mucosa, enterotoxin
Clinical: gastroenteritis followingcontaminated seafood ingestion
Immune response: stomach acid kills it; inflammatory response to enterotoxin, Igsonce infected
Treatment and/or prevention:symptomatic treatment with fluid and electrolytereplenishment, as it is a self-limited infection
Epidemiology:45,000 cases/year;
Timing: 24 hour incubation, 1-7 day duration;
Vibrio parahaemolyticusalso causes a watery diarrhea. Therecan be fever and some bloodiness to it, as V.parahaemolyticuscan be invasive, as compared to cholera.
Vibrio cholerae
Pathogen category: G-curved rod, aerobic, extracellular
Source: human reservoir, can exist in fresh water
Virulence factors: adhesion to intestinal epithelium, flagella for motility for spreading; cholera- toxin driven
Clinical: cholera
Immune response: stomach acid kills it; Igsonce infected
Treatment and/or prevention:rehydration; doxycycline or azithromycin
Epidemiology:1.3 to 4 million cases/year; with estimated range of 20,000-140,000 deaths/year; https://www.who.int/en/news-room/fact-sheets/detail/cholera
Timing:0.5 to 5 days incubation, can kill within hours without rehydration; WHO
Vibrio cholerae: a Gram-negative curved, flagellated rod. acid sensitive require large dose for it to occur. The choleraexotoxin greatly increases enterocyte secretion via irreversible activation of adenylyl cyclase and subsequent high cAMP stimulation of CFTR, so a painless rice-watery diarrhea that can lead to shock and death by dehydration. key feature of treatment is rehydration (ORT- salt-sugar water combination to enhance absorptioin) doxy and zithromycin for shortening disease course and controllingw ater and sewer control.
vulnificus- working in salt water, diabetes, and wound causing infections
salt water toxin- rest can live in salt water.
vibrae- freshwater
vibriae- paralyticus eat not fully cooked seafood watery and tinge of blood diarrhea
incubation of 1 to 2 days, fever and cramps, followed by watery diarrhea that can then turn bloody. gram -. under endoscope develop white splotches
what is it?
what is the pathogen category? normal colonic flora? virulence factors? clinical? immune response? treatment and/or prevention? describe how it works in general and the particular strains that cause damage
Shigellaspecies
Pathogen category: G-rod, aerobic, intracellular
Source: human reservoir
Virulence factors: Shigatoxin; stomach acid resistance; invasion plasmid antigens
Clinical: shigellosis
Immune response: inflammatory response with neutrophils, Igssubsequent to infection
Treatment and/or prevention:ciprofloxacin
Shigellaspecies also generate a bloody diarrhea or dysentery. Features of interest:
- Gram-negative,nonmotilerods treatable with fluoroquinolones
- low dose of pathogen needed (as compared to Salmonella)
- incubation of 1 to 2 days, fever and cramps, followed by watery diarrhea that can then turn bloody (note the intestinal invasion in the colonoscopeimage).
- Shiga toxin is an AB-type toxin that inactivates ribosomal function.
- Localized battle in the peyerspatch developpingpockets of pus developing infiltrates all the way through developing
S. sonneileads to a mild disease in this country, e.g., during the summer with young children (less than 5 years old). S. dysenteriaegenerates a more severe illness in developingcountries.
may show up as right lower quadrant pain mimicing appendicitis with painfully swollen lymph nodes. watery/bloody diarrhea
what is it?
what is the pathogen category? normal colonic flora? virulence factors? clinical? immune response? treatment and/or prevention? describe how it works in general and the particular strains that cause damage
Yersinia enterocolitica
Pathogen category: G-rod, aerobic, extracellular
Source: animal reservoir;ingestion of infected cold meat, milk
Virulence factors: coldtolerance- ; YadA(Yersiniaadhesin A) binds anticomplementproteins; Yop(Yersiniaouter proteins) injected to inhibit macrophage secretion and trigger cell apoptosis
Clinical: watery/blooddiarrhea; regional adenitis
Immune response: inflammatoryresponse with neutrophils; Igsonce infected
Treatment and/or prevention:oftennone; doxycycline and gentamicin if sepsis
Epidemiology:120,000 cases/year in US; https://www.cdc.gov/yersinia/faq.html
Timing: 4-7 days after exposure; 1-3 weeks of disease; https://www.cdc.gov/yersinia/faq.html
Yersinia enterocoliticainfection, although uncommon,can mimic appendicitis, as it infects terminal ileum and mesenteric lymph nodes. Gram-negative rod, can be treated with doxycycline combined with aminoglycoside if severe (Sanford Guide).
- requires large load of bacteria to generate an infection
- cold-tolerantso can appear in contaminated, refrigerated meat or dairyproducts
- Exotoxin- kill off local immune cells not having battle at mucosa or loose connective tissue but can go to the local lymph node prolieratingto those activities.
Once at 37o, thepathogen injects Yops(Yersiniaouter proteins), which despite their name, act as exotoxins that decrease phagocytosis and other macrophage functions, allowing the pathogen to spread and proliferate in lymph nodes and have them swell painfully.
consumption of meat leading to diarrhea
what is it?
what is the pathogen category? normal colonic flora? virulence factors? clinical? immune response? treatment and/or prevention? describe how it works in general and the particular strains that cause damage
Clostridium perfringens: consumption of the spores in meat can lead to a fairly common diarrhea (as vs. a gas gangrene).
initially watery diarrhea may progress to full-blown colitis.
treat w/ metronidazole, vancomycin (high concentration to kill it off and not impacting normal gram - flora). gram + rod.
what is it?
what is the pathogen category? normal colonic flora? virulence factors? clinical? immune response? treatment and/or prevention? describe how it works in general and the particular strains that cause damage
Clostridium difficile
Pathogen category: G+rod, obligate anaerobe, extracellular
Source: gut flora, can outgrow other flora with antibiotics, nosocomial
Virulence factors:endospore formation, toxin A as enterotoxin, toxin B as cytotoxin
Clinical: pseudomembranous colitis
Immune response:normal flora
Treatment and/or prevention:metronidazole (anaeorbic specialist damaging DNA), vancomycin; fecal transplant if recurrent
Epidemiology:450,000 cases/yearin US with 30,000 deaths;
Timing: usually after 1 week of antibiotics, with abrupt onset of diarrhea
Clostridium difficilefeatures:
- Gram-positive rod, anaerobic, spore-forming, normal inhabitant of the GI tract
- implicated in antibiotic-associated diarrhea; avoid broad-spectrum antibiotics if possible
- with overgrowth, C. difficilereleases exotoxinsthat bind to and stops protein synthesis and kill enterocytes, with resulting pseudomembraneproduction
- initially watery diarrhea may progress to full-blown colitis
- spores can spread the disease; wash those hands with soap and water!
- screen feces with ELISA for toxin
Difficult to treat, with antibiotic cessation and infection control (wash hands, minimize spore spread), treatable with vancomycin as standard options, with metronidazole less popular, particularly for the severely ill or infirm. Given the challenge of C. diff infections, additional items of fidaxomicin (RNA polymerase inhibitor) as expensive alternative drug. For recurrent infection, fecal microbiota transplant (FMT) is more effective than vancomycin. Bezlotoxumab(monoclonal antibody against the B toxin) was approved by the FDA in 2016 as an agent to lessen recurrence.
triggers vomiting (rarely diarrhea) within 3-6 hours of consumption of contaminated food that is usually protein-rich
what is it? What is produced by this? How is it caused? How do you treat it and prevent spread?
Staphylococcus aureusgenerates a number of exotoxins. The one that you might be most familiar with is enterotoxin A that triggers vomiting (rarely diarrhea) within 3-6 hours of consumption of contaminated food that is usually protein-rich. Wash those hands prior to food preparation!
Thestaphylococcalenterotoxin A that generates such a rapid response acts as a superantigenwhich triggers a lot of nonspecific activity in the lamina propriaof the intestines. enhance interact w/ T cells and MHC. bursts of immune mediators in the connective tissue
produces gastritis that can develop into peptic ulcer disease, and can contribute to gastric cancer
what is it?
what is the pathogen category? normal colonic flora? virulence factors? clinical? immune response? treatment and/or prevention? describe how it works in general and the particular strains that cause damage
Helicobacter pylori
Pathogen category: G-curved rod, microaerophilic, extracellular
Source: human reservoir
Virulence factors: urease
Clinical: gastritis, peptic ulcer
Immune response: inflammatory response once in mucosa
Treatment and/or prevention:With clarithromycin resistance, quadruple therapy withbismuth, tetracycline, metronidazole, and PPI. Can treat statically, gram -, and protect epithelium from further damage w/ peptobismol added
Epidemiology:positive serology rangesfrom 30% of Dutch blood donors to 95% of Nigerians with dyspepsia;
Timing:difficult to identify, with chronic infections that may be asymptomatic.
Helicobacter pylori: a Gram-negative curved rod that can generate a gastritisassociated with peptic ulcer.
Ureaseto generate buffering, adhesive molecules to attach, and injectable exotoxins to generate cell damage of urea. The urease activity is the basis for a number of sensitive tests for H. pylori. Pathogen adheres w/ pili, give off exotoxin to damage cells and make a food source.
This combinationof persistence and invasion can trigger inflammation and lead to peptic ulcer diseaseor even gastric cancer.
patient has abdominal pain and has been found to have abscesses around the body located outside large intestine (diverticulitis), lower right quadrant (appendicitis), in the lung (lung aspiration), dental infection. gram -
what is it?
what is the pathogen category? normal colonic flora? virulence factors? clinical? immune response? treatment and/or prevention? describe how it works in general and the particular strains that cause damage
Bacteriodesfragilis
Pathogen category: G-rod, obligate anaerobe, extracellular
Source: #1 normal colonic flora
Virulence factors:capsule, collagenase
Clinical: intra-abdominal abscesses, bacteremia
Immune response:Ig to capsule during sepsis, complement, cell-mediated immunity and neutrophils during abscesses
Treatment and/or prevention:debridement, metronidazole (with 3rdgeneration cephalosporin to cover other G-enteric bacteria in abscess)
Epidemiology:anaerobescan be identified in 10% of blood cultures taken;
Timing: diverticulitis should improve within 2-3 days of treatment
Bacteroidesfragilis: the most common inhabitant of the colon. Bacteroide sand other anaerobes can generate abscesses with foul-smellingcontents—note the deep oral, pelvic, and abdominal locations of the anaerobes.
•Gram-negative pleomorphic rod, treatable with metronidazole
polysaccharide capsule andbeta lactamase production arevirulence factors, with an abscess indicatinga cell-mediated response to try to clear the infection
patient complains of abdominal pain, is found to have a gram negative abdominal infections, heart murmur and chest pain when breathing, as well as pain when urinating
what is it?
what is the pathogen category? normal colonic flora? virulence factors? clinical? immune response? treatment and/or prevention? describe how it works in general and the particular strains that cause damage
Enterococcus species (E. faecium, E. faecalis)
Pathogen category: Gram-positive coccus, facultative anaerobes
Source: human reservoir,normal flora
Virulence factors: multiple drug resistance, including vancomycin; biofilm; pili
Clinical: intra-abdominal infections, endocarditis, urinary tract infections
Immune response: neutrophils, macrophages, complement
Treatment and/or prevention:depends on resistancepatterns; penicillinsfor sensitive strains vs. additional MRSA-type drugs, e.g., linezolid, vs. addition of aminoglycosides for synergism in endocarditis
Epidemiology:one of the most common pathogensfor nosocomial infections; https://emedicine.medscape.com/article/216993-overview#a6; 10% of endocarditis;
Timing: incubation period unknown;
Enterococcus speciesare a common part of the intestinal flora, but have been increasingly recognized as pathogens, particularly in nosocomial situations in patients having extensive antibiotic exposure. As mentioned before the break, recent chemical modification of vancomycin to (eventually) address enterococcal resistance, although not to market for a while. nosocomial infection if out of the barrier of the GI have speciialized feature including adherance and biofiliming with toxin release destroying tissue they are biofilmed on developing endocarditis.
patient particularly young child develops a virally found vomiting and diarrhea.
what is it?
what is the pathogen category? normal colonic flora? virulence factors? clinical? immune response? treatment and/or prevention? describe how it works in general and the particular strains that cause damage
Rotavirus
Pathogen category: ds RNAunenvelopedvirus
Source: human reservoirs; stable in environment
Virulence factors: double-shelled capsid (usually cant make it past bile) only ones that can
Clinical: gastroenteritis in children
Immune response: cell-mediated and humoral immunity
Treatment and/or prevention:live oral vaccine; symptomatic treatment if infected
Epidemiology:followingvaccination patterns, rotavirus now rare in US
Timing:1-3 day incubation, 4-8 days of diarrhea
The gastroenteritis virusesare unenveloped, allowing them to be more resistant to environmental conditions, including the detergent-like effect of bile that would degrade a phospholipid envelope. Two major examples are the reoviruseswith rotavirus and caliciviruseswith norovirus.
Rotavirusis a segmented, ds RNA virus that has the protection of an outer capsid layer that get broken down during its trip in the digestive system, but allows it to survive the acidity of the stomach. The diarrhealillness occurs at the tips of intestinal villi, and so triggers both a bit of malabsorptionas well as triggering of the enteric nervous system that lead to the diarrhea and vomiting consistent with the illness. Fast replication and antigenic drift (from the error-prone RNA polymerase) allow some avoidance of the immune system.
The current rotavirus vaccine is a live, attenuated virus scheduled for infant dosing.
Antibodiesto rotavirus can occur, hence rotavirus tends to be an early childhood diarrhea.
patient is on a cruise and develops muscle aches, gneeral sense of fatigue, leading to vomiting and is a viral origin
what is it?
what is the pathogen category? normal colonic flora? virulence factors? clinical? immune response? treatment and/or prevention? describe how it works in general and the particular strains that cause damage
Norovirus
Pathogen category: +ssRNA unenvelopedvirus
Source: human reservoirs; stable in environment
Virulence factors: fewvirions required for infection (e.g., 10); multiple strains
Clinical: gastroenteritis
Immune response: apparentlycell-mediated and humoral immunity, butshort-lived
Treatment and/or prevention:hand washing and preventionof exposure; supportivecare; oral fecal spread
Epidemiology:20,000,000cases/year in US; https://www.cdc.gov/norovirus/php/illness-outbreaks.html
Timing:24-48 hour incubation, symptoms 12-60 hours (Current 2019)
Calicivirusesare +ssRNA viruses similar to the picornaviruses. Norwalk virus(norovirus) is a common cause of diarrhea (“winter vomiting illness”) that can be seen in groups, with an oral-fecal spread as it is a very environmentallyhardy virus. There is a1-2 day incubation, 1-3 day symptoms, and several weeks ofadditional viral shedding. It appears to trigger villus blunting (via epithelial cell apoptosis), loss of brush border enzyme function, and some leakage of tight junctions at the villi for the diarrheal aspects and delayed gastric emptying for the vomiting aspects of this “stomach flu” (Khan, 2018).
Washing those hands is the best preventative measure,as multiple strains and (in contrast to rotavirus) the lack of long-term immunity will mean that individuals remain susceptible to re-infection.
hit and strain run, leaky, quick stimulation of lamina propria (connective tissue beneath the epithelium),
shellfish is contaminated w/ sewage and is eaten raw, (+) ss RNA picornavirus (i.e., unenveloped) virus. It is spread oral-fecally and causes inflammation of the liver
what is it?
what is the pathogen category? normal colonic flora? virulence factors? clinical? immune response? treatment and/or prevention? describe how it works in general and the particular strains that cause damage
Hepatitis Ais a (+) ss RNA picornavirus (i.e., unenveloped) virus.
It is spread oral-fecally, and can persist in dried feces (or shellfish). Once taken up by M cells in the Peyer patches, HAV gets taken into the liver and then has a period of infection. igg permanent memory cytotoxic t clears it, w/ circulating antibodies stopping any delivery into the portal circulation
HepatitisA virus
Pathogen category: unenveloped+ ssRNApicornavirus
Source: contaminated food products
Virulence factors: environmentalhardiness
Immune response: strong cell-mediated response that destroysthe infected liver cells and humoral response for clearance of viremia
Treatment and/or prevention:vaccine; immune globulin
Epidemiology:with vaccination in the US, 2000 cases in 2016; with risk of international travel, more common overseas (much of population having infection in childhood).
Timing:onset 3 weeks after exposure, acute illness for 2-3 weeks (Current 2019)
Using the graph describe the virulsence and infection of hepatitis B.
what is it?
what is the pathogen category? normal colonic flora? virulence factors? clinical? immune response? treatment and/or prevention? describe how it works in general and the particular strains that cause damage? describe the infection pathway.
Hepatitis Bis an incomplete ds DNA enveloped virus(Hepadnavirusfamily) with a more complicated life cycle strategy compared to HAV, as it uses reverse transcriptase to generate the DNA. Much of its activity involves the surface antigen(HBsAg), which as seen in this image,is made in excessive quantities.
HepatitisB virus
Pathogen category: envelopedds DNA hepadnavirus
Source: human reservoir blood-borne, sexual
Virulence factors: extensive production of surfaceantigens- dominant feature of enveloped virus (cheese doodles) lots of core antigen and capsid protein- not a complete loop of dna(pretends it’s a dnavirus but uses reverse transcriptase)
Clinical: hepatitis B
Immune response: strong cell-mediated response that destroysthe infected liver cells and humoral response for clearance of viremia and future prevention
Treatment and/or prevention:vaccine; immune globulin; reverse transcriptase inhibitors
Epidemiology:with vaccination in the US, childhood rates should be dropping, with 3200 acute cases in US reported to CDC in 2016 and estimation of 21,000 cases vs, those reported; much more common overseas;
Timing:4 weeks after exposure, 2-3 weeks of acute illness, recovery by 16 weeks
HBsAb(IgG-antiHBs; antibodies to HBsAg) will be protective,but you need high enough titers of antibodies to address all of the “empty” HBsAgnot associated with the virions (Dane particles).
Developing anti-antiboodycomplexes-type 3. w/ core antigen and capsid proteins makes it difficult to make antibodies against since it is buried in the surface antigen. glomerular nephritis, joint pain
The core antigen generates antibodies as well, but these are not protective. HBeAgis a secreted antigen that is derivedfrom the core protein HBcAg, andin effect acts as another immune decoy. HBeAgindicates active disease and infectivity.
Thewindow where it doesnt look like there is anthing happening between anti-HBe, represents where the patient is clearing the infection but may not yet show the protective HBsAb, as the HBsAgand HBSAbare titrating each other off.
Formany, there is sufficient specific immune response to kill of the HBVvirus via aCTL response to clear the infected liver As liver cells die, there less capacity to handle bilirubin, leading to jaundice seen in hepatitis patients. cells. HBV antigen-antibody complexes may cause type III hypersensitivities in the skin/joints/kidney.
In other patients, achronic illness occurs, where the chronicinflammation can be a risk factor for hepatocellular carcinoma.
very high transmission.
is a kind of long term chronic hepatitis
what is it?
what is the pathogen category? normal colonic flora? virulence factors? clinical? immune response? treatment and/or prevention? describe how it works in general and the particular strains that cause damage
Hepatitisc virus
Pathogen category: enveloped+ssRNA flavivirus
Source: human reservoir
Virulence factors: error-prone RNApolymerase and establishment of variable populations
Clinical: hepatitis C
Immune response: humoral response that does not typically clear infection
Treatment and/or prevention:sofosbuvir, lepidasvir, and related medications;
Epidemiology:3000 new cases reported to CDC in 2016, with estimation of actual 41,000 new cases; vs. 2.4 million in US withchroicinfection
Timing:6-7 week incubation; 80% with chronic disease (Current 2019)
HCVis a +ss RNA flaviviru sthat is notorious for different genotypes and an error-prone RNA polymerase generating a variable population of virus in an infected individual. A personmay generate HCV Abs, but most clearance occurs through CTLs.
Given this difficulty in clearingHCV, most (80+%) infected individuals will go onto to chronic disease (note the lymphoid infiltrate in the liver sample).
Different genotypesof HCV have different response rates to therapy. Briefly, there are 6 genotypes, with 1 and its subtypes the most common, and the hardest to treat. Recommendations have been undergoing many changes in the last few years:
A brief history of where HCV meds came from:
Mainstay for 2000s:
Ribavirin: a nucleoside analogthatcan inhibit RNA polymerase activity. It can be tried in a number of severe RNA viral infections and was used in combination with interferon alphathat has been pegylated(bound up with polyethylene glycol) to addressHCV, albeit with a large number of side effects leadig to a lack of compliance.
Introduced in 2011, first generation serine protease inhibitors, e.g., boceprevir, to prevent the cleavage of a synthesized polyprotein into separate proteins, were used to target the common HCV 1 genotype. These added to anemia and other issues that ribavirin and interferon contributed to, so the first generation serine protease inhibitors are no longer recommended for HCV.
Current therapy (2014à)
Sofosbuvir is a prodrug with good oral bioavailabilty that, after the first pass effect in the liver, becomes a very effective nucleoside antagonist to the HCV RNA polymerase. Its high level of effectiveness, its cost, and the possible extent of the population it can effect all combine to make current and future HCV treatment trends controversial.
Lepidasvir and more recent medications, e.g., velpatasvir,inhibit a nonstructural protein 5A (NS5A) whichinteractswith the NS5B RNA polymerase that sofosbuvirtargets. As a result, combination therapy is the norm for HCV. inhibitting non-cyclovering proteins
Second generation protease inhibitors such as grazoprevir are offered in combination with the NS5A medications as current treatment options for HCV.
many different genotypes then starts establishing multi-variable population due to error prnone protein kinase leading to targetting in many different directions
what makes hep. d so dangerous?
what is it?
what is the pathogen category? normal colonic flora? virulence factors? clinical? immune response? treatment and/or prevention? describe how it works in general and the particular strains that cause damage
HepatitisD virus
Pathogen category: enveloped(via HBV) ssRNA deltavirus
Source: human reservoir
Virulence factors: co-infection with HBV
Clinical: hepatitis B/D superinfection
Immune response: some cell-mediated and humoralresponse
Treatment and/or prevention:control of HBV infection
Epidemiology:rarein USA; 15 millionpeople worldwide (~5% of HBV-infected population), particularly Mediterranean region;
Timing:similar to HBV, but may be shorter with superinfection;
HepatitisDis unusual in that it is an incomplete ssRNAvirus that requiresthe presence of HBV for envelopment.When HDV co-infects with hepatitis B, it can worsenthe hepatitis, presumably by replicating in liver cells and directly damaging them. Usually only an add on to Hepb and can go from clearing infection to not clearing .
therefore treat hep. B then Hep. d cannot be completed and you are cureed
this hepatitis is a major killer of pregnanywomen in many different poored regions
what is it?
what is the pathogen category? normal colonic flora? virulence factors? clinical? immune response? treatment and/or prevention? describe how it works in general and the particular strains that cause damage
HepatitisE virus
Pathogen category: unenveloped+ssRNA hepevirus
Source: human reservoir, oral-fecal spread, more among adults than children
Virulence factors: can be fatalin pregnant women
Clinical: acute hepatitis
Immune response: cell-mediatedand adaptiveresponse
Treatment and/or prevention:water-foodprecautions; HEV vaccine approved in China in 2012, but not available/approved in USA
Epidemiology:diseaserarein USA; 20 millionpeople infected worldwide each year, with 3.3 million infections and with 44,000 deaths in 2015;
Timing:5-6 week incubation; WHO
hepatitis Eis more common overseas than in the USA. It is a +ssRNA hepevirus(formerlyplaced with calicivirus) that has a disease pattern similar to that of hepatitis A. particularly common in pregnant women making them a vulnerable population.
what is it?
what is the pathogen category? normal colonic flora? virulence factors? clinical? immune response? treatment and/or prevention? describe how it works in general and the particular strains that cause damage
Entamoebahistolytica
Pathogen category: ameba
Source: human reservoir, oral-fecal spread
Virulence factors: cysts
Clinical: ambeiasisfromtrophozoites
Immune response: eosinophilic, not neutrophils or macrophages
Treatment and/or prevention:avoidanceof contaminated food; metronidazole for trophozoite, paromomycin for cyst
Epidemiology:300 cases/year in US; worldwide: 50,000,000 with invasive disease and 100,000 deaths annually; Timing: 2-4 week incubation, with 1-2 week gradual onset colitis
Entamoebahistolyticais a world-wide cause of amoebic dysentery that has oral-fecalspread by cysts.
Dysentery results as Entamoeba trophozoitesburrow into large intestinal walls and causes flask-shaped ulcers. Liver and lung abscesses can also appear as the organism gets swept up by the portal circulation to the liver and then with extension from the superior surfaceof the liver to the lungs.
need to kill off cysts and trophozoite Metronidazole or the similar product tinidazole will help to take care of the trophozoite. For a situation where a patient is passing cysts, paramomycinor iodoquinolis needed. Paramomycin, an aminoglycoside, and iodoquinol, a quinolone, are poorly absorbed and so reaches high concentrations in the gut. These two are specialty access drugs in the US.
sharkoladin crystals utilizing eosinophils to break it down.
hiker drinks fresh mountain stream and develops diarrhea, steatorrhea, what do they have?
what is it?
what is the pathogen category? normal colonic flora? virulence factors? clinical? immune response? treatment and/or prevention? describe how it works in general and the particular strains that cause damage
Pathogen category: binucleateflagellate
Source: animal reservoir (stream drinking);human reservoir possible
Virulence factors: large numbers,adhesive disk that affects mucosa
Clinical: malabsorptivediarrhea (not absorbing fat creating steatorhea)
Immune response: cell-mediatedresponse
Treatment and/or prevention:water treatment;metronidazole or tinidazole (fewer doses per day)
Epidemiology:5000 hospitalizationsannually;high in other parts ofthe world, e.g., 10% prevalence in many parts (Current 2019)
Timing:1-3 week or longer incubation; symptoms may continue for weeks to months.
Giardialamblia (G.intestinalis, G. duodenalis):flagellate found in water contaminated by human or animal sources that canmultiply rapidly by binary fission as a trophozoitein the small intestine. From inhaling cysts and develops flagellates (against peristalsis) attaching in the small intestine,altering function of villi. concentrate of destroying trophozoite since they reproduce leave cysts
waves of flare up of diarrhea due to bad foods ex. strawberries doctor gave a bunch of antibiotics and nothing worked difficult to stain but found acid fast staining and that sulfa drugs works doing ova and parsite test.
what is it?
what is the pathogen category? normal colonic flora? virulence factors? clinical? immune response? treatment and/or prevention? describe how it works in general and the particular strains that cause damage
Cyclosporacayetanensis
Pathogen category: coccidian(sporozoan) protozoan
Source: environmental, from contaminatedfood or water
Virulence factors: disruptionof small intestinal epithelium
Clinical: watery diarrhea
Immune response: cell-mediatedresponse to clear
Treatment and/or prevention:water-foodprecautions; sulfa drugs
ThesporozoanCyclosporacayetanesisis spread by ingestion of its oocystsfrom contaminated food, with a first major outbreak in the USA seen in 1996 with imported Guatemalan raspberries (low number of organismsneeded for infection). Visualization of oocysts for diagnosis (PCR not fully available for clinical use). Trimethoprim-sulfamethoxazole is the current medication of choice.
Cycloisospora(Isospora) belli
Pathogen category: coccidian(sporozoan) protozoan
Source: environmental, from contaminatedfood or water
Virulence factors: disruptionof small intestinal epithelium
Clinical: watery diarrhea
Immune response: cell-mediatedresponse to clear
Treatment and/or prevention:water-foodprecautions; sulfa drugs, antiretroviral therapy
Cystoisospora(Isospora) belli is included here as a very similar pathogen to Cyclospora, also treatable with sulfa meds, but like Cryptosporidiumin that it impacts patients with AIDS.
patient develops a pneumonitis then begins to develop nausea, vomiting, abdominal discomfort and pain, loss of appetite
what is it?
what is the pathogen category? normal colonic flora? virulence factors? clinical? immune response? treatment and/or prevention? describe how it works in general and the particular strains that cause damage
roundworms thrash from giant intestinal
Phylum Nematoda: roundworms, with a complete mouth to anus gut, a muscular pharynx, and a protective cuticle. A pseudocoelfilled with fluid creates a hydrostatic skeleton that allows a characteristic thrashing motion in roundworms as they contract their longitudinal muscles. larva penetrate bloodstream and can end up in capillary bed ex. lungs (pneumonitis), goin through several larval stages in order to get cuticle of the roundworm to protect it from environment due to hacking up and then is ingested into the large intestine. eggs ingested larva maturing in the lungs then adult into the intestine. eggs can also go in through the feet if walking through entering bloodstream and into lungs.
The microtubule-altering drug albendazole(or the similar mebendazole, recently returned to the US market) is generally indicated for nematodes, as this preferentially interferes with microtubule-based activities such as glucose uptake in the worms (the process may take a few days to expel the worms). These medications are expensive. As a result, the OTC meds of Reese’s Pinworm Medicine with pyrantel pamoate are increasingly in favor (pyrantel pamoate as a neuromuscular depolarizing blocking agent to paralyze the worms and allow them to be defecated).
pinworm annoying, hookworm and ascaris are potentially deadly.
what is the pathogen category? normal colonic flora? virulence factors? clinical? immune response? treatment and/or prevention? describe how it works in general and the particular strains that cause damage
Ascarislumbricoides
Pathogen category: nematode (roundworm)
Source: human reservoir, oral-fecal spread
Virulence factors: cuticle; highrate of egg production
Clinical: eosinophilicpneumonitis in larval stage; other asymptomatic or mechanical effects
Immune response: IgEand eosinophils (Th2-based response)
Treatment and/or prevention:water-foodprecautions; albendazole or mebendazole with pyrantel pamoate alternative
Epidemiology: 1%prevalenceinUS, mostly the Southeast; 1 billion infected worldwide
Timing:typically asymptomatic, adult worms live for 1-2 years
Ascarislumbricoides, theintestinal roundworm. Adults live in the small intestine, lay lots of eggs (thousands per day) in the feces, and the larva starts forming in the eggs. When the (infective) eggs are swallowed, they hatch, the larva penetrate the intestine and are carried up to the lung. They then crawl up the trachea, are swallowed, and reach maturity in the intestine.
Common worldwide; in the US, Ascariswould be most often seen in rural Southeast. Ascarisinfestations, if in low numbers, do not create much problem, but mechanical obstructioncan occur if the worms are sufficiently numerous.
what is the pathogen category? normal colonic flora? virulence factors? clinical? immune response? treatment and/or prevention? describe how it works in general and the particular strains that cause damage
Enterobiusvermicularis
Pathogen category: nematode (roundworm)
Source: human reservoir, oral-fecal spread
Virulence factors: cuticle; high rate ofeggproduction
Clinical: asymptomaticor anal region pruritis
Immune response: IgEand eosinophils(Th2-basedresponse)
Treatment and/or prevention:careful laundering of infectedbedding and clothing; albendazole (treat 2 weeks later ot make sure hasnt rehatched) or pyrantel pamoate
Epidemiology: 40,000,000inUS; ~10% prevalence worldwide (Current 2019)
Timing:1-2 month maturation of female after egg ingestion (Current 2019)
Enterobiusvermicularis, the human pinworm, is the most common roundworm parasite in the USA, with a life cycle revolving around the large intestine. Females come out at night of the anus to lay eggs nearby. The associated pruritusleads to scratching and oral reinfection. Treating the patient and others in the house, and thoroughly laundering bedding and clothing, are all indicated.
Thescotch tape test highlight the distinctive eggs collected from their perianallocation.
live in large intestine keeping life cycle laying eggs on perianal folds, female crawls out and lays egg itching their butt and autoinocculate repeating this cycle.
patients feel drained, can causes severe anemia
what is the pathogen category? normal colonic flora? virulence factors? clinical? immune response? treatment and/or prevention? describe how it works in general and the particular strains that cause damaget
Hookworm,e.g., Necatoramericanus
Pathogen category: nematode (roundworm)
Source: human reservoir, spread from infectedsoil
Virulence factors: cuticle; cutting blades in mouth
Clinical: asymptomatic;anemia
Immune response: IgEand eosinophils (Th2-based response)
Treatment and/or prevention:footwearin potentially contaminated soils; albendazole (not officially approved in US for hookworm,but reasonable) or pyrantel pamoate; ironreplacement
Epidemiology: rareinUS; 500 million people worldwide with 65,000 deaths/year (Current 2019)
Timing:adult worms last 1-2 years; overall infection can persist for years.
Necatoramericanus, the New World hookworm. Hookworm is a disease of warmer, damp climates, as the larval form hatches in fecallyinfected soil and penetrates the skin of the bare foot. The visualization of eggs in the stool should allow for diagnosis. The anterior end of the adult hookworm forms a “hook” that is used to latch onto a small intestinal villus to feed on blood, causing severe anemia.
southeast US, eggs are defecated on the ground, wak around barefoot penetrating in the lungs.
bad diet, poorly cooked pork and can develop new onset seizures.
what is the pathogen category? normal colonic flora? virulence factors? clinical? immune response? treatment and/or prevention? describe how it works in general and the particular strains that cause damage
Tapeworms- sacs of gonads.Fold in on itself and corssfertilize.
Taeniaspecies
Pathogen category: tapeworm (classof flatworms)
Source: zoonotic (fish-7-8 meter and beef)
Virulence factors: highlevels of reproductive capacity
Clinical: mostly asymptomatic, or vague GI symptoms
Immune response: some eosinophilia
Treatment and/or prevention:cooking meat; praziquantel-trgger calcium influx, muscle contraction forcing antigenic feature of worm that is uaulyl blandly immunologic will allow them to come out and be recognized by immune system. (along with albendazole and prednisone for neurocysticercosis- bladder worms in the brain
Epidemiology:about 2000 hospitalizations/yearin US for neurocysticercosis, particularly among Hispanics; 20% of children in endemic areas such as South America can be infested with Hymenolepis
Timing:variable timing; neurocysticercosistypically presents with new onset seizures;
Cestoda(tapeworms)are specialized intestinal helminths. They can be long (up to 10 meters with the broad fish tapeworm Diphyllobothrium) and ribbon-like. They are composed of rectangular shaped reproductive units known as proglottids. Each proglottidis able to function independently. Adult tapeworms attach to the gut wall with their scolex. can develop vitamin B 12 levels w/out enough nutrients from large worm.
The tapeworm life cycle involves ingestion of infected meat via a bladder worm (cysticercusstage), with the attachment of the scolexin the small intestine, and the growth of proglottidsfull of eggs, which then can pass in the feces. Taeniasolium, the pork tapeworm, is considered more dangerous, as occasionally the eggs hatch in the small intestine and the larvae encyst in the body, e.g., generating neurocysticerosis.
Praziquantelis the drug of choice for (most) tapeworms (and flukes), as it binds to a flatworm calcium channel to trigger an influx of calcium that causes muscle contraction and paralysis as well as tegument disruption with new antigen exposure.
pork tate worm- eggs penetrate and circulate to musculature if bladder worm in muscle similar presentation to trichomonas
someone eats wheat when the food is cooled and then reheated developing short spell of vomiting, watery diarrhea. gram positive.
what is it?
what is the pathogen category? normal colonic flora? virulence factors? clinical? immune response? treatment and/or prevention? describe how it works in general and the particular strains that cause damage
Bacillus cereus
Pathogen category: G+rod, aerobic, extracellular
Source: soil and contaminated food
Virulence factors:endospore, enterotoxin
Clinical: food poisoning, often with reheated rice
Immune response:macrophage response generated, not alwayseffective, against the bacterium
Treatment and/or prevention:symptomatic
Epidemiology: probably common, underreportedcause of food poisonings in multiple countries, possible 30,000 to 60,000 year in the US; https://www.gideononline.com/2011/12/10/bacillus-cereus-food-poisoning-in-the-united-states/
Timing: 10-16 hours, 24-48 hours of watery diarrhea (Current 2019)
Bacillus cereus. Features of interest:
- aerobic Gram-positive rod, spore-forming, found in grains
- spores survive cooking, then germinate with a heat-stabile enterotoxinwhen the grains (e.g., rice) are held at warm temperatures, and generate rapid-onset vomiting
- other toxins may generate more of limited, watery diarrhea (similar to but not as extensive as cholera)
What are the strategies in difference in the hepatitis viruses?
- HAV, HEV: oral-fecal, shorter incubation, no carrier state
- HBV, HCV, HDV: parenteral spread, longer incubation, more chance of carrier state.
oral-fecal spread of HAV and HEV with short incubation and no carriage state, vs. the blood-borne exposure of HBV, HCV, and HDV, with a longer incubation and stronger likelihood of chronic illness.
describe the graphical represenation of HBV.
What protozans infect the small and large intestine?
what worms ingest the small and large intestine?
most worms in small intestine because there is more food and nutrients
what is it?
what is the pathogen category? normal colonic flora? virulence factors? clinical? immune response? treatment and/or prevention? describe how it works in general and the particular strains that cause damage
Trichuristrichiura
Pathogen category: nematode (roundworm)
Source: human reservoir, oral-fecal spread
Virulence factors: cuticle; high rate ofeggproduction
Clinical: asymptomatic; diarrhea or tenesmus
Immune response: IgEand eosinophils (Th2-basedresponse)
Treatment and/or prevention:avoidance of infected soils or foods; albendazole or ivermectin
Epidemiology: 700,000,000world-wide; (presumably) several hundred thousand in the Southern US;
Timing:eggs take 3 weeks in soil before infectious;
Trichuristrichiura, the human whipworm, is verycommon in developing countries, with infestations triggering a chronic diarrhea, or if the worm load is high enough, a sufficient sense of tenesmus that can lead to rectal prolapse. The anterior part of the worm will anchorin the large intestinal epithelium, with the posterior parts protruding, as seen in the slide image.
similar life cycle and it hangs out in the colon pentrating first half buried in the mucosa can cause prolact of rectum due to larger worm load
what is it?
what is the pathogen category? normal colonic flora? virulence factors? clinical? immune response? treatment and/or prevention? describe how it works in general and the particular strains that cause damage
Strongyloidesstercoralis
Pathogen category: nematode (roundworm)
Source: human reservoir, spread from infectedsoil
Virulence factors: cuticle;hyperinfectionsyndrome (larval penetration of mucosa)
Clinical: asymptomatic;watery diarrhea; hyperinfectionin those with low Th1 counts (AIDS patients)
Immune response: cell-mediated immunity to prevent hyperinfection
Treatment and/or prevention:footwearin potentially contaminated soils; water-foodprecautions; ivermectin- interferes w/ invertebrate neurotransmission paralyzing it disabling worm
Epidemiology: 4% infection rate inSouthern US; 100-200 million worldwide;
Timing:infection can persist for decades if unrecognized;
larvae mature in immune compromised can develop autoinfection penetrating right away w/ a heavy wormload in tissues right away a lot more lethal
Strongyloidesstercoralis, the threadworm, also can penetrate a foot and mature initially in the lung like hookworm. The female lays eggs along the bowel wall rather than the lumen, so that the larval forms hatch and penetrate the intestinal wall of the host to generate an autoinfection, which can lead to a hyperinfectionsyndrome in the immunocompromised. Ivermectin(targets invertebrate chloride channels to trigger Cl-influx, with subsequent hyperpolarization, and hence, nerve and muscle dysfunction) would be considered the first line choice for Strongyloides, with albendazoleas an lesser alternative.
common in hunter and farmer develops infection and causes death in many pigs with body pain.
Trichinellaspiralis- pork worm
Pathogen category: nematode (roundworm)
Source: animal reservoirs,spread by undercooked meat (pork or wild game such as bear)
Virulence factors: cuticle; highrate of egg production
Clinical: eosinophilicpneumonitis in larval stage; other asymptomatic or mechanical effects
Immune response: IgEand eosinophils (Th2-based response)
Treatment and/or prevention:meat cooking, as freezing does not always work; albendazole with prednisone to lessen inflammatory response
Epidemiology: 13 casesin US in 2015, mostly from eating undercooked wild animal meat; require cook meat in high temp.
Timing:abdominal symptoms 1-2 days after eating infected meat; additional symptoms 2-8 weeks later;
Trichinellaspiralisis a nematode whose larval form encysts, and then is taken up in poorly cooked meat. The larvae then can hatch, mature, release larvae that then penetrate the intestine to get carried to muscles to encyst. While the USA had high rates for much of the 20thcentury (500 cases/year still reported to the CDC in the 1940s), better awareness has decreased this.
