1 - Microbiology

Question 0

What are common oral pathogens? What are the common presentations?

Answer 0

1) Streptococcus pyrogens (gr +, diplococci, coagulase +, beta hemolytic/clear) -> acute pharyngitis, scarlet fever (rash), impetigo, cellulitis, necrotizing fasciitis, Strep Toxic Shock Syndrome–> can lead to rheumatic fever, acute glomerulonephritis, bacterial endocarditis
2) Staph aureus (gr +, diplococci, coagulase -) -> lip ulcers (mucositits) and stomatits
3) Herpes (1=oral, 2=genital; icosahedral capsid, lin dsDNA) -> oral lesions, ulcers and cauliflowers
4) Coxsackievirus/hand-foot-mouth (ssRNA, small) -> presents as herpangina on the hand/foot/mouth in children and immunocompromised; enterovirus spread through fecal-oral
5) HPV -> STI that presents as pappillomas in the mouth/tongue; major cause of squamous, esophageal cx
6) Canida (yeast or hyphal(infectious) forms) normal flora, pathogenic in immunocompromised -> thrush or yeast infections

Question 1

What are some common Oral Flora?

Answer 1

1) many species of anaerobes
2) Strep Viridans (gr +, diplocci, coagulase +, alpha hemolytic/green) -> cause of dental caries
3) Lactobacilli (gr +, rod, facultative anaerobe, forms lactic acid) -> associated w/ cavities and dental carries
4) Neisseria spp.
5) Diptheroids (nonpathogenic cornybacteria)
6) Mycoplasms
7) Spirochetes

Question 2

What are some common causes of esophagitis?

Answer 2

1) GERD
2) Allergies: eosinophilic esophagitis
3) Infectious esophagitis: more common in immunocompromised
- Herpes: seen in bone marrow/solid organ transplants
- HPV/CMV: seen in bone marrow transplants
- Canidia: more common w/ HIV

Question 3

What are common gastric pathogens?

Answer 3

1) Heliobacter pylori (gm -, rod/spiral, facultative aerobe, Urease +)
2) HSV/CMV -> think immunocompromised population

Question 4

Describe Helobacter pylorui.

Answer 4

1) Gr -, rod/sprial shaped, facultative aerobe, Urease +
2) Pathogenesis: binds to gastric mucosa and induces an acute inflammatory rxn-> causes mucosal damage -> develops into chronic gastritis -> becomes Chronic Atrophic Gastritis -> Gastric Carcinoma
3) Virulence Factors: urease, Vac A, Cag A
- Urease: breaks urea into CO2 and NH4+ which raises the gastric pH and helps H.pylori survive in stomach
- Vac A: vacuolating cytotoxin attacks the mitochondria to make it permeable -> helps inhibit T-cell activation
- Cag A: Cag pathogenicity island is “injectable” into the cell and modulates several cell pathways; also seen to be an Oncogene

Question 5

How is H. pylori infection diagnosed? Tx?

Answer 5

1) Glemsa or Wurthin-Starry stain
2) urease/pH test -> turns yellow to red as pH increase
3) culture
4) breath test -> breath out CO2, NH4+ and urease
5) antibody test
TX: Triple therapy = Proton Pump Inhibitor + 2 Ab
1) omeprazole
2) lansoprazole
3) bismuth subsalicylate

Question 6

Describe Shigella GI infections.

Answer 6

1) Enterobacteriaceae: gr (-), rods, ferment glucose, oxidase (-)
- Shigella dysenteriae: most severe type and more common in under-developed countries -> produces Shiga Toxin
- Shigella flexnerii: most common in under-developed countries
- Shigella sonnei: most common in U.S.
- Shigella biydii: rare
2) Symptoms: presents as a range of disease from asymptomatic to watery diarrhea to colonic dysentery -> abdominal pain, fever, stools = low volume, bloody, mucoid, w/ Fecal Leukocytes
3) Shiga Toxin (shigella dysenteriae) can produce Reiter’s Syndrome (polyarthritis) and Hemolytic Uremic Syndrome
4) Pathogenesis: bacteria enter through M-Cells; eaten by mac’s and cause mac apoptosis; enter the basolateral enterocyte and replicate in Cytoplasm; invade neighbors via actin polymers
5) Epidemiology: Highly Infectious (Feces, Fingers, Fomites, Fly Feet); invasive at warmer (body) temps; common to close living quarters and poor hygiene (Cruise Ships, POWcamps, Water Park, Day Care, Prisons..)
6) Dx: Culture, stain of fecal leukocytes, Lactoferrin (quantitative from PMN granules)

Question 7

Describe Salmonella Non-Typhoidal GI infections.

Answer 7

1) Enterobacteriaceae: gr(-), rods, glucose fermenters, oxidase (-)
2) S. enteritidis, S. typhimurium, S. heidelburg -> zoonotic, causes Enterocolitis or Sustained Bacteremia (in elderly and infants)
3) Enterocolitis:
- Symptoms: 8-48hr incubate, abrupt onset w/ low fever, nausea, vomiting, Watery Diarrhea; lasts 2-5d
- Pathogenesis: ingestion of contaminated food/water -> colonization on small intestine -> invasion of epithelium -> multiplication in endosome w/o destruction -> PMN activated (IL-8)
4) Bacteremia
- Symptoms: variable incubation, abrupt onset w/ Rapid High (septic) fever, few other GI symptoms; variable duration
- Pathogenesis: -Pathogenesis: ingestion of contaminated food/water -> colonization on small intestine -> invasion of epithelium -> multiplication in endosome w/o destruction -> invasion of bloodstream -> focal lesions in lungs, bones, heart, etc
* *can progress to septic shock -> LPS/LipA
5) Common Sources: eggs (50%), unpasteurized milk, meat, vegetables

Question 8

Describe typhoidal salmonella infection.

Answer 8

1) Enterobacteriaceae: gr (-), rod, glucose fermenter, oxidase (-)
2) S. typhi, S. paratyphi -> only in humans and leads to Typhoid Fever
3) Symptoms: incubate 7-20d, insidious onset w/ a gradual rising fever to a high plateau (typhoidal state), early constipation, later bloody diarrhea; lasts several weeks
4) Pathogenesis: ingestion of contaminated food/water -> colonization in small intestine -> invasion THROUGH M-Cells/Peyer’s Patches -> replicate in macs and travel in bloodstream to form focal lesions throughout the body
5) Virulence Factors: Capsule (not in non-typhoidal), survives in mac’s, can exist in carrier state
6) Vaccine: 1) whole cell killed -> poor efficacy; 2) Attenuated Live/ Purified Capsule Antigen -> high efficacy + cost

Question 9

Describe Yersinia GI infections.

Answer 9

1) Enterobacteriaceae: gr (-), rods, glucose fermenters, oxidase (-)
2) Y. pseudotuberculosis, Y. enterocoltica: zoonotic (pigs); high in Europe/Scandanavia -> grown well at 4C
3) Enterocolitis: fever, abdominal pain, inflammatory diarrhea; can progress to Reiter’s Syndrome: polyarthritis
4) Mesenteric Lymphadenitis: mimic appendicitis
5) Entraintestinal infections (less common)

Question 10

Describe Eschericia coli GI infections.

Answer 10

1) Enterobacteriaceae: gr (-), rods, LACTOSE fermenters, oxidase (-)
2) ETEC, EIEC, and EPEC present as Secretory diarrhea, no fecal PMNs, no blood,
A) ETEC: characterized as Traveler’s diarrhea and Children’s diarrhea -> common in Troops in Africa/ME
-Pathogenesis: ingestion of contaminated food/water -> colonization of small intestine -> release enterotoxins LT (temp labile) and ST (temp stable) -> cause raise in cAMP/cGMP, which cause a high osmotic gradient and a lots of water (diarrhea)
B) EIEC: presents like shigella w/ symptoms ranging from watery diarrhea to dysentery -> common in children
C) EPEC: acute and chronic diarrhea in children form attaching/effacing lesions via Pathogenicity Island (PAI) -> release Shiga toxin -> binds Gb3 on glomeruli and inhibit protein synthesis -> destruction of glomerular cells and decreased GFR -> ARF
-Hemolytic Uremic Syndrome: when antibiotics are given to tx STECs there is a higher risk that the shiga-producing bacteriophage is stimulated into lytic phase and begins to replicate -> rapid increase in toxin and rapid HUS
4) Epidemiology: zoonotic transmission, LOW infectious dose -> common of Water Parks, Day Care, Instiutions
5) Prevent: cook meat (>160F), wash vegetables, pastuerize milk/juice,
6) Dx: ELISA, PCR

Question 11

Describe Campylobacter jejuni GI infections.

Answer 11

• • Top cause of bacterial diarrhea in US
    1) Gm (-), tiny gull-shaped rods, microaerophilic, oxidase (+)
    2) Zoonotic: birds and others
    3) Inflammatory Diarrhea: PMNs, cramps, bloody diarrhea (late)
    4) Complications: Guillain Barre Syndrome (auto-immume respose from cross-reaction between LPS core and myelin); Reiter’s Syndrome (reactive poly-arthritis, urinary tract, eyes, skin, mucus membranes)
    5) Dx: CAMPE plate -> stool/blood @ 42C in atmosphere w/ less O2 and more CO2

Question 12

Describe Vibrionaceae GI infections.

Answer 12

1) V. cholerae, V. parahaemolyticus: gm (-), comma-shaped rods, glucose fermenter, oxidase (+)
2) Cholerae: serotype O1(Classical and El Tor) and O139 cause epidemic and pandemic cholera; others cause Cholera-like diarrhea, mild diarrhea or extra-intestinal infections
- profuse watery (rice water) diarrhea, vomiting and leg cramps (hypokalemia); can progress to hypovolemic shock -> low BP, weak pulse, sunken eyes, poor eye turgor, hyperventilation
- Pathogenesis: colonization of small intestine via Toxin Co-Regulated Pili (Tcp Pili) -> releases cholera toxin which activates cAMP/cGMP -> altered Na/Cl gradient causing massive water excretion -> rice water diarrhea
- Risk Factors: young children, travelers w/o immunity, blood group O
- Vaccines: killed whole cell, live attenuated
3) Parahemolyticus: acute watery diarrhea, occasional blood, severe cramping, abdominal pain, SHORT (15hrs)
- Pathogenesis: similar to cholera but produces Thermostable (direct) Hemolysin (Tdh)
- Epidemiology: uncooked seafood (oysters), common in Japan
4) Dx: agar plate for culture
5) Tx: Rehydration

Question 13

Describe Clostridium difficile GI infection.

Answer 13

• *most common cause of nosocomial diarrhea
  1) gr(+), rod, Spore forming, anaerobe
  2) Pathogenesis: part of the normal flora of ~1% of population or exposed in hospital environment, but overgrows other flora to become pathogenic in the presence of antibiotic therapy -> invade enterocytes -> elaborates Toxin A (necrotizing cytotoxin) and Toxin B (disaggregation of actin filaments) -> causes white “psuedomembranous” plaques and necrosis
  3) Symptoms: ranges from mild diarrhea to severe, necrotizing infection of colon
  4) Dx: toxin testing (cytotoxic assay, PCR), stool culture (high false positive)
  5) Tx: STOP the antibiotics, give metronidazole/vancomyacin as indicated; fecal transplant

Question 14

What are the types of food borne illness?

Answer 14

1) Intoxication by pre-formed toxin in food: Clostridium botulinum, Staph aureus, Bacillus cereus
- incubation time: 1-6hrs
2) Intoxications caused by toxins manufactured by the body: Clostridium perfringes, E. coli, Vibrio cholerae
- incubation time: 8-12hrs
3) Intestinal invasive disease: salmonella, campylobacter jejuni.
- incubation time: 8-48 hrs

Question 15

Describe the common bacterial GI infections associated with pre-formed toxins.

Answer 15

1) Clostridium botulinum: spores contaminate food (canned, smoked) -> spores germinated @ high pH -> in anaerobic conditions vegetative form grows and releases botulism toxin -> toxin is absorbed by small intestine/stomach -> interrupts ACh uptake at NMJ -> flaccid paralysis
2) Staph aureus: superantigen secreted by staph binds to MHCII APC and T-cells to cause unregulated release of inflamatory cytokines (IFN-g, TNF-a) -> cause vomiting (more) and diarrhea
3) Bacillus cereus: Emetic form is caused by a heat stable enterotoxin (rice, incubation 1-6hr); Diarrheal form is caused by infection by bacteria and secondary secretion of heat labile enterotoxin (meat, vegetables, sauces; incubation 8-24hrs)

Question 16

Describe GI infection by Rotavirus.

Answer 16

1) Rotavirus: dsDNA, non-enveloped, incosahedral/double shelled, segmented genome -> reassortment between species; replication in cytoplasm
2) Infectious after VP4 capsid enzyme is cleaved by GI enzymes
3) Epidemiology: causes infantile ( damage to Na/Cl channels cause osmotic (watery) diarrhea -> when enterocyte dies it releases large viral load
5) Symptoms: incubation 1-2d, watery diarrhea, vomiting, mucus in stool, severe dehydration
6) Dx: ELISA, antibody titer, RT-PCR
7) Tx: supportive therapy
8) Vaccine: Rotarix -> human G1 strain, Rotateq -> reassorted strain from 4human and 1bovine

Question 17

Describe GI infection by Norovirus/Norwalk Virus?

Answer 17

• • leading cause of food borne disease in US
    1) Norovirus: +ssRNA, non-enveloped, icosahedral, replication in cytoplasm
    2) Very Stable: heat resistant, resistant to chlorine -> shellfish, pools
    3) Epidemiology: more common in older children/adults, but can occur at any age; fecal-oral spread via contaminated food -> cruise ships, schools,
    4) Pathogenesis: infection of small intestine leads to Broadening and Blunting of villi in proximal sm. intestine -> cellular inflammation and cytoplasmic vacuolization lead to malabsorption
    5) Symptoms: Sudden Onset, nausea, vomiting, abdominal cramps, fever, chills -> Diarrhea = watery, non-bloody, no-mucous
• largely self limited w/ complications rising from severe dehydration
  6) Dx: symptom based, no fecal leukocytes, PCR, antigen detection, rapid tests (less sensitive)
  7) Tx: electrolyte replacement

Question 18

Describe the GI infection by Adenovirus.

Answer 18

1) Enteric adenovirus 40/41: linear dsDNA, non-enveloped, icosahedral, replicates in nucleus
2) Pathogenesis: infects mucoepithelial cells via CAR receptor -> persists in lymphoid tissue (Peyer’s patches) -> temporal replication (immediate early, early and late)
3) Epidemiology: primarily infects young children via fecal-oral transmission and lasts 1-2wks
4) Dx: PCR, ELISA, symptoms
5) Tx: supportive
4)

Question 19

Describe the general characteristics of picornaviruses. What are some pathogenic examples?

Answer 19

1) Picornaviridae enterovirus: (+)ssRNA, non-enveloped, icosahedral
2) VERY stable: resistant to heat, drying, 70% ethanol, 5% lysol
3) Replication cycle: virus binds to the membrane (ICAM-1) and is uncoated/released into cytoplasm -> translation begins and polyprotein is cleaved to produce viral proteins -> +RNA is copied by the virus’ RNA Polymerase to -RNA -> -RNA is then copied to produce additional +RNA -> virus particles are lysed from cell
4) Coxsackievirus A: diffuse myositis w/ acute inflammation and necrosis of voluntary muscles; Hand-Foot-and-Mouth dx; meningitis; herpangina; encephalitis; hemorrhagic conjunctivitis
5) Coxsackievirus B: focal areas of degeneration in the brain and necrosis of skeletal muscles; encephalitis; myocarditis; pancreatitis/diabetes I; neonatal disease;
6) Poliovirus: 3 serotypes; present as progressive paralytic disease
7) Echovirus: highly infectious of children; acute febrile illness than can develop into aseptic meningitis, paralysis, myocarditis, measles-like rash
8) Dx: Cox B and Echo are readily grown in culture, but Cox A is NOT -> PCR

Question 20

Describe the distinguishing characteristics of the different herpetic viruses.

Answer 20

1) Genome: dsDNA=HBV; ssRNA=HAV, HCV, HDV, HEV
2) Enveloped: HAV, HEV
3) Transmission: Enteric=HAV, HEV; Parenteral/Perinatal/Sex =HBV, HCV, HDV
4) Acute?: HAV, HEV, ~HCV
5) Chronic/HCC?: HBV, HCV, HDV

Question 21

Describe hepatitis A virus.

Answer 21

1) HAV: ssRNA, non-enveloped, icosahedral
2) enteric transmission (fecal-oral) via contaminated food/water
3) Can cause acute illness (2-6wks post infection): fever, fatigue, nausea, vomiting, loss of appetite, abdominal pain, icteric hepatitis
4) does NOT cause chronic hepatitis or confer increased risk of HCC
5) Dx: HAV-IgM = current infection; HAV-IgG = immunized (>5wks)

Question 22

Describe hepatitis E virus.

Answer 22

1) HEV: ssRNA, non-enveloped, icosahedral
2) enteric transmission (fecal-oral) via contaminated water
3) causes an acute illness: fever, nausea, vomiting, abdominal pain, jaundice
4) Pregnant Women -> HEV can be abortive and/or fatal
5) Dx: IgM-HEV = current infection; IgG-HEV = immunization (>5wks)

Question 23

Describe Hepatitis B Virus.

Answer 23

1) HBV: dsDNA, enveloped, icosahedral
2) HBV is non-cytolitic, but causes cell death from CTL activation
3) can produce Chronic Hepatitis and increases risk for HCC
4) infected cell releases both infectious particles and non-infectious patricles/filaments -> all contain HBsAg
5) Transmission: parenteral, perinatal, sexual -> blood is highly infectious -> common STD and nosocomial
6) Lab: HBsAg = current infection; anti-HBc IgM=acute infection; anti-HBc IgG=past/chronic infection; HBsAb = past infection/immunization; HBeAg/HBV-DNA = active replication; Anti-HBe = no longer replicating
7) Tx: INF alpha; Lamivudine (reverse transcriptase inhibitor)
* *successful tx = seroconversion of HBsAg/HBV-DNA disappear and HBsAb and anti-HBe develop

Question 24

Describe Hepatitis D Virus.

Answer 24

1) is a defective virus which requires the surface proteins of HBV to survive
2) Coinfection w/HBV: acute disease w/ little risk of chronic infection
3) Superinfection w/HBV: rapid onset can present as fulminant hepatitis w/ encephalopathy; high risk of developing into chronic hepatitis
4) Transmission: parenteral, sex, IV drug use

Question 25

Describe Hepatitis C Virus.

Answer 25

1) ssRNA, enveloped, icosahedral
2) presents as acute hepatitis (2-26wks; 7-8 typical) -> 70% persist chronically; 15% recover; 15% rapid cirrhosis
3) genome is highly variable, so there is no immunity or vaccine
4) Transmission: parenteral, perinatal, sexual -> blood transfusion, IV drug use, hemodyalysis
5) Dx: anti-HCV core protein (not in acute phase), HCV-RNA (track therapy progress)
6) Tx: pegylated INF alpha, ribavirin (used as adjunct)

Question 26

Describe the infection by Entamoena histolytica.

Answer 26

1) Entamoeba Histolytica is a protozoan parasite that infects humans via invasion of trophozoites into intestinal and extra-intestinal tissue
2) Intestinal Pathogenesis: spread through fecal-oral transmission via contaminated food/water -> mature cyst releases trophozoite which invades intestinal tissue -> secretes enzymes to lyse mucosa down to muscular layer -> develops Flask-Shaped ulcers in the Cecum, Sigmoid, and Hepatic/Splenic flexures
3) Intestinal Symptoms: variable incubation period leading to Dysentery (bloody, mucoid diarrhea); acutely presents as etloss, abdominal pain, tenesmus and fever; chronically presents as constipation alternating w/ diarrhea -> can develop lactose intolerance
4) Extra-intestinal Path: begins as intestinal amebiasis then ulcers may perforate the bowel and enter peritoneal cavity, may spread to portal circulation and invest distant organs -> forms sterile abscesses in liver, brain, kidney, genitalia, skin
5) Extra-intestinal Symp: based on the infected organ; Liver-> RUQ pain, fever, hepatomegaly, mass; Lung -> cough, bloody sputum w/ trophozoites
6) Dx: direct ID from mucous/stool; needle aspiration of extra-intestinal abscess
7) Tx: Metronidazole; Tinidazole, Paromomycin

Question 27

Describe infection by Giadia lamblia.

Answer 27

• • most prevalent intestinal parasite in US
    1) Flagellates that are commonly transmitted via contaminated water; cysts can survive for months in even chlorinated water
    2) Symptoms: ranges from asymptomatic to acute, explosive diarrhea and malabsorption; acutely presents as diarrhea, abdominal pain, bloating, nausea, vomiting, flatulance, steatorrhea; Chronically presents as wt loss, malabsorption, and debilitation
    3) Dx: direct microscopy (trophites w/ two nuclei and flagella); ELISA
    4) Tx: metronidazole, tinidazole, nitazoxanide, quinacrine, furazaolidone

Question 28

Describe Cryptosporidium parvum.

Answer 28

1) Intestinal protazoan parasite; fecal-oral transmission via contaminated water/food (pools/cider)
2) Presents as watery diarrhea, vomiting, abdominal pain
3) can be asymptomatic, self-limiting, or wasting and fatal if immunocompromised
4) Tx: primarily supportive; immunocompromised can use HART or nitazoxanide

Question 29

Describe Cyclospora cayetanesis.

Answer 29

1) protozoan parasite that is common in tropical/subtropical area (Nepal)
2) transmission is fecal-oral via contaminated water fresh produce (berries)
3) incubation period of ~1wk, presents as watery diarrhea, anorexia, wt loss, abdominal pain, nausea, vomiting, mylaise, low fever and fatigue -> lasts 10-12wks untreated
4) Tc: trimethoprin, septra

Question 30

What trematodes and cestodes cause intestinal disease?

Answer 30

1) Trematodes (flukes) -> Fasciolopsis buski
- acquired from aquatic vegetation (water chestnuts) and develop in the sm. intestine over 3mo
- presents w/ diarrhea, fever, abdominal pain, ulceration and hemorrage
- Dx: eggs in stool; Tx: praziquantel
2) Cestodes (tapeworms) -> Taenia saginatum, Taenia sodium, Diphyllobothrium latum
- acquired from contaminated beef (saginatum), pork (solium) and fish (D.latum)
* * Taenia solium eggs can cause neurocystercycosis
- Dx: proglottids and eggs in stool; Tx: praziquantel

Question 31

What is neurocysticercosis?

Answer 31

1) eggs from Taenia solium (tapeworm from pork) are ingested, they are absorbed by the intestine and travel to the brain, muscles and/or eyes -> lesions form around cyst due to inflammatory rxn
2) presents as seizures, hydrocephalus, headaches, focal neurological deficits
3) Dx: imaging, biopsy, serology
4) Tx: praziquantel +/- corticosteroids; surgical removal

Question 32

Describe Ascaris.

Answer 32

• *most common helminth infection
  1) large, non-segmented roundworm that infects primarily children in developing countries
  2) Symptoms: most are asymptomatic, but children w/ small bowels can present w/ abdominal discomfort/distention, biliary/pancreatic obstruction; Loeffler’s Syndrome: eosinophilic pneumonitis caused by migration to lung -> dry cough, dyspnea, eosinophilia
  3) Dx: though eggs are found in stool due to high number produced, they do not present until 2-3mo after pulmonary symptoms
  4) Tx: lung infection is self-limiting, GI -> mebendazole, albendazole

Question 33

Describe hookworm.

Answer 33

1) Necator americanus, Ancylostoma duodenale: blood-sucking roundworms that can pass THROUGH THE SKIN and shows a high prevalence in teenage/young adult males
2) Particularly dangerous for females/pregnant women due to the affect of anemia -> cause fetal retardation, low birth weight, stunting
3) Symptoms: iron deficient anemia, pneumonitis (wheezing, dyspnea, dry cough), urticarial rash
4) Dx: eggs in stool
5) Tx: mebendazole, albendazole

Question 34

Describe Trichuris.

Answer 34

1) Trichuris (whip worm) is both intra/extracellular roundworm that predominately affects children
2) Eggs are ingested, hatch and migrate to cecum where they mature
3) Symptoms: large number of worms can mimic Ulcerative Colitis (bloody, mucoid diarrhea w/ abdominal pain); can develop into rectal prolapse
4) In children -> impaired growth, anemia and clubbing of fingers
5) Dx: O/P (football egg, doubly operculated)
6) Tx: albendazole, mebendazole, ivermectin

Question 35

Describe Strongyloides stercoralis.

Answer 35

1) Strongyloides can live both free and as parasite and can infect by passing THROUGH THE SKIN and can persist for DECADES in the body
2) 50% are symptomatic -> diarrhea, abdominal pain, nausea, vomiting, heartburn; Invasive -> occult blood, brief diarrhea, brief constipation; Pulmonary -> wheezing, transient infiltrates; Skin -> urticarial rashes, larva currens (migrating patterns)
3) Larvae are secreted in stool, so unlikely to be picked up on O/P
4) Hyperinfection Syndrome: if immunocompromised or very large parasitic burden -> gram negative sepsis, fever, hypotension, meningitis, pneumonitis
5) Dx: O/P (low; larvae hard to see), serology, culture

Question 36

Describe Enterobius vermicularis.

Answer 36

1) Enterobius vermicularis (pinworm) is a common infection of tropical areas (children>adults) which is transmitted fecal-oral
2) Symptoms: frequently asymptomatic, but can present as peri-anal itching
3) Dx: O/P (poor; squished football eggs)
4) Tx: mebendazole, pyrantel, pamoate, piperazine, ivermectin

Question 37

Describe opisthochiidae.

Answer 37

1) Opisthorchis viverrini and Clonorchis sinesis are liver flukes that are common to Asia/SE Asia
2) Life Cycle: eggs from human feces -> ingested by snails -> free swimming larvae is released by snail and eaten by Carp -> metacercaria develops in Carp and is ingested by human -> invests and matures in the bile duct
3) flukes persist in bile ducts causing significant inflammation and fibrosis, bile duct proliferation -> squamous metaplasia -> cholangiocarcinoma, recurrent ascending chalangitis/pancreatitis
4) Symptoms: Acute (rare)-> fever, Eosinophilia, abdominal pain, fatigue, hepatomegaly; Chronic -> abdominal pain, fatigue, hepatomegaly, dyspepsia
5) Dx: O/P @ 3-4wks (lid at one end, knob at the other); Ultrasound
6) Tx: praziquantel, albendazole

Question 38

Describe fasciola hepatica.

Answer 38

1) Fasciola hepatica is a liver fluke that is seen anywhere sheep/cows are farmed; Fasciola gigantica -> subsaharan Africa
2) Life cycle: eggs from human/animal feces ingested by snail -> metacercaria live independently on water vegetations (watercress) -> ingested by cows/sheep and eggs excreted in feces -> ingested by humans and is absorbed by intestine -> burrows through intestine wall into the peritoneal cavity and liver
3) Symptoms: Acute Hepatic (Invasive) Stage -> (6wk to 4mo post infection) abdominal pain, intermittent fever, wt loss, malaise Eosinophilia
- Chronic Biliary (Obstructive) Stage -> (flukes in lumen) intermittent abdominal pain, biliary obstruction, ascending cholangitis, jaundice, lithiasis
4) Dx: O/P, antibody test, CT, Ultrasound
5) Tx: Triclabendazole, Bithionol,

Question 39

Describe Schistosoma.

Answer 39

1) Schistosoma mansoni (Africa, Middle East, S. America), Schistosoma japonicum (east asia) are blood flukes that have separate male/female sexes
2) Life Cycle: eggs in feces/urine -> ingested by snail -> cercaria released by snail and is infectious directly through skin -> enters circulation and mature (mansoni = portal) -> secrete egg pouches that digest through gut wall -> are expelled or reabsorbed -> eggs in liver can cause aseptic granulomas (pipe-stem fibrosis)
3) peri-portal fibrosis causes portal hypertension -> esophageal/umbilical varices, hepato/splenomegaly, ascities
4) Symptoms: progressive (mo->yrs), fatigue, abdominal cramps, RUQ pain, Bloody Diarrhea, iron deficient anemia, portal hypertension –> hepatic function frequently preserved
5) Acute Schisto -> seen in patients from non-endemic areas (military/travelers); abdominal pain, FEVER, headache, diarrhea, eosinophilia -> fatal?
6) Dx: O/P (large egg w/ prominent lateral spine), ultrasound, serology
7) Tx: Praziquantel