HIV

Q: Describe HIV.
A: It is an enveloped, diploid, + sense ssRNA virus

Q: What enzymes are packaged in the HIV virion?
A: Reverse Transcriptase, Integrase, and Protease

Q: What is the difference between HIV-1 and HIV-2?
A: HIV-1 is found worldwide. HIV-2 is mainly found in west Africa (less transmittable).

Q: How do most neonates get HIV?
A: Most commonly intrapartum (during labor), then transplacental, then postpartum (i.e. breast feeding).

Q: How do HIV enter cell?
A: gp120 of HIV bind to CD4 of the host cell. Then a co-receptor on the host cell binds (CCR5 in macrophages, CXCR4 in Th cells)

Q: How does HIV enter body?
A: Enters through mucosal surface. Then picked up by dendritic (Langerhans) Cells, which move them to lymph nodes.

Q: How long after infection is HIV fond in the lymph nodes? In plasma?
A: 2 days in lymph node, 5 days in plasma (so starts becoming infectious)

Q: What are the stages of HIV infection?
A:
Stage A = Primary Infection (1-3 weeks)
Stage B = Symptomatic HIV Disease
Stage C = AIDS
Stage 1 = >500 cell count
Stage 2 = between 500 – 200 cell count
Stage 3 = <200 cell count

Q: What are the symptoms when the HIV virus first infects (Stage A)?
A: First of all, most people will not have any symptoms. But if there are symptoms, remember HIV will first infects lymphoid organs and CNS (microglial cells) – so you get maculopapular rash and flu-like signs and symptoms. Viral concentration drops by 3-6 months.

Q: What cells are depleted and downregulated by HIV infection?
A: macrophages, CD4+ T-cells, CD8+ T-cells.

Q: What are the genes in the HIV-1 Genome and what do they encode?
A:
Gag – group-specific antigen gene – so encodes viral nucleocapsid protein.
Pol – polymerase gene – so encodes protease, reverse transcriptase, integrase
Env – envelope gene – so encodes gp120, which is a glycoprotein found on the envelope. (Actual it encodes gp160 which splits into gp120 and gp41).
Tat – transactivator of transcription gene – encodes transactivator
Rev – regulator of virion gene – protein that transport RNA to cytoplasm
Nef – negative factor – downregulates MHC I on host cells, so infected Th4 can’t activate CTL and be killed.

Q: What is p17? p31? p41?
A:
p17 = gag
p31 = integrase
p41 = env

Q: What are the signs and symptoms of HIV Stage B?
A: Stage B is the symptomatic stage. You get swollen lymph nodes, lack of energy, weight loss, and frequent fevers. You start getting opportunistic infections, like long-lasting diarrhea, frequent yeast infections, shingles, or persistent skin rashes from the normal flora on your body. KEYWORDS: More frequent and More persistent infections.

Q: What are some conditions associated with HIV Stage B?
A: BASICALLY ANYTHING THAT HAS TO DO WITH NORMAL FLORA
Bacillary angiomatosis — angiomas caused by bacteria
Persistent Oral thrush or Genital Candidiasis — caused by Candida on your body.
Persistent Diarrhea, like that caused by Cryptosporidium
Hairy Leukoplakia — white patches on side of tongue with hairy appearance due to lytic destruction of epithelial cells — Epstein-Barr Virus
Listeriosis — listeria infection, whcih remember causes meningitis.

Q: What is CDC’s definition of AIDS?
A: HIV+ with fewer than 200 CD4+ T-cells per cubic millimeter of blood, as well as having multiple opportunistic infections.

Q: What are some conditions you see with HIV Stage C (last stage now called AIDS)?
A: Wasting syndrome (loss of more than 10% of your weight, due to all that diarrhea and what not), Encephalopathy (remember HIV infects CNS) — confusion, seizures.

Q: What is Kaposi’s Sarcoma?
A: malignancy of blood vessels seen in AIDS patients. You get grape-like lesions on skin.

Q: What measure is used to stage disease?
A: CD4+ T-cell count… duh

Q: What are the two major classification systems used in staging HIV’s progression?
A: CDC and WHO.

Q: Describe the CDC’s way of classifying what is “AIDS.”
A: basically, if you have a CD4 cell count of less than 200, even if you have no symptoms of AIDS, you have AIDS according to the CDC. If you have AIDS symptoms but have a high T-cell count above 200, you still have AIDS.

Q: How do you screen for HIV?
A: use ELISA.

Q: How do you confirm HIV?
A: use Western Blot to detect antibodies (made by patient) against pol or env proteins. You could also use PCR to find reverse transcriptase (RT-PCR).

Q: WHat would indicate a positive result for HIV?
A: if you detect gp41 + gp120/160 OR p24 + gp120/160

Q: What is used to test HIV in blood donors?
A: p24 detection… an early marker of infection… so used for blood donors and rape victims.

Q: What is the “window period”?
A: Period of time in which the patient has HIV but does not show it in their serum. usually around 3-4 weeks.

Q: During the progression of HIV infection, what markers will show up in order?
A: HIV RNA will be detected earliest after infection, followed by HIV p24, then antibodies against HIV (i.e. anti-env antibody).

Q: What are the five classes of anti-retroviral drugs (against HIV)?
A:
RTI — Reverse Transcriptase Inhibitor
PI — Protease Inhibitor — Indinavir, Ritonavir, Nelfinavir (remember “Navir Tease”?)
FI — Fusion Inhibitor — Enfuvirtide (remember “enFUvirtide”)
Maraviroc — CCR5 Co-Receptor Antagonist — Maraviroc (remember MAraviroc = MAcrophage)
InSTIs — HIV Integration Inhibitor — Raltegravir (remember inTEGRAte = ralTEGRAvir)

Q: What are the two types of RTIs (reverse transcriptase inhibitors)?
A:
NRTIs — nucleoside RTI — AZT, Lamivudine, Abacavir
NNRTIs — non-nucleoside — Delavirdine, Nevirapine

Q: What is HAART (highly active antiretroviral treatment)?
A: It’s a combo treatment with at least 2 NRTIs + 1 PI

Q: According to the International AIDS Society, when should we treat an HIV+ patient?
A: When they are already symptomatic of HIV disease (Stage B) and/or if their T-cell count is less than 200 (even if they are asymptomatic). Treatment should also be considered if HIV-1 RNA is greater than 100,000 copies/ml. If cell count between 200-350, consider treatment. For everything else, don’t treat.

Q: An HIV+ mother is going to have a baby. What do you do?
A: give the other anti-HIV drugs, as well as the baby once it’s born. Do a C-section… lowers chance of infecti
on to baby. DO NOT BREAST FEED! unless you live in a country where everyone’s starving.

Q: Why shouldn’t we use nonoxynol-9 (contraceptive) or cellulose sulfate (microbicide)?
A: Because they have been shown to actually increase risk of infection!

Q: Statistically in the US, what sex, ethnicity, age, region have the highest case of HIV infection?
A: black, male, 30s, the south/new york/nevada/colorado

Q: What is the most common way of transmission of HIV in males vs. females?
A: Males — homosexual contact; Females — heterosexual contact

Q: What are some other quick-and-easy tests you can do for HIV?
A: Dried Blood Spot, OraQuick Saliva Test, Calypte Urine Test, Wellcozyme Vaginal Secretion Test.

ENDOCARDITIS

Q: How does endocarditis present?
A: inflammation of the endocardium. Has vegetations on surface or inside endocardium, most commonly in the heart valve. Vegetations interfere with the physiology function.

Q: What kind of patients should you suspect has endocarditis?
A: patient with fever of more than several days and heart murmur (because of the vegetations). Night sweats, weight loss.

Q: What are some additional features of endocarditis?
A:
Splinter Hemorrhages — clots (from vegetations) cause breakage in nails.
Conjunctival hemorrhages — also from clots from vegetations caught in conjunctival vessels –> inflammation
Osler Nodes — little nodules on fingers. broken vegetations get lodged in fingers. bacteria infect here –> septal embolism.
Janeway Lesions — hemorrhagic lesions on soles of feet. they will blanch.
Clubbing of Fingers — due to low oxygenation in tissue –> thickening of soft tissue, causes fingers to curve.

Q: What is the age for endocarditis?
A: middle age (47-60)

Q: Who has the highest risk of endocarditis?
A: people with predisposing conditions, like artificial heart valves, congenital heart defects, etc.

Q: How do we treat endocarditis?
A: try to reduce the risk, like if you go to dentist, have anaprophylaxis nearby in case reaction to bacteria… risk stratification

Q: What are the steps that cause endocarditis?
A: bacteria in blood stream –> flow to heart –> bacteria adhere to valves and other parts of endocardium –> infection forms vegetations

Q: Where do you most commonly find vegetations (most infected part of endocardium)?
A: bicuspid, except in intravenous drug users, which is tricuspid

Q: What are the three groups that cause endocarditis?
A: Strep, Staph, HACEK

STAPHYLOCOCCUS

Q: What two species of staphylococcus cause endocarditis?
A: S. aureus and S. epidermidis

Q: Intravenous drug users have predominantly what bacteria?
A: Staph. aureus

Q: People with catheters and other indwelling lines and who get endocarditis, what is the most common infection?
A: Staph. aureus

Q: What is the most predominant staph species on our skin?
A: Staph epidermis, so can also spread to endocardium with cuts.

STREPTOCOCCUS VIRIDANS

Q: What lancefield is Strep. viridans?
A: NONE!

Q: What kinda capsule does it have?
A: Dextran-like capsule

Q: Where do you find Strep viridans?
A: It is normal flora in oropharynx. So you can get it into blood stream with dental procedures.

Q: Who is at risk?
A: people who have had dental or other invasive procedures.

Q: What is the clinical disease for viridans?
A: Endocarditis, duh.

Q: What are characteristics of the HACEK organisms?
A: They are gram negative rods (only gram negatives causing endocarditis), normal flora, VERY SLOW GROWING!!! often called “culture negative” because so slow.

Q: What are the HACEK organisms?
A:
H — Hemophilus species
A — Actinobacillus
C — Cardiobacterium
E — Eikenella
K — Kingella (though now reclassified as aggrecan whatever)

MYOCARDITIS

Q: Describe myocarditis.
A: Inflammation of muscular wall of heart… so you get abnormal beats. Heart becomes thick and swollen — Dilated Cardiomyopathy.

Q: Who is at risk of myocarditis?
A: middle-aged men, average 42 yrs old. people who recently have viral illness (cause autoimmune response).

Q: How do myocarditis patients present?
A: tachycardia, inefficient pumping of heart, dysrhythmia.

Q: What is the best way to diagnose myocarditis?
A: biopsy

Q: How do you treat myocarditis?
A: treat associated illness, drugs that help the heart pump during illness.

TRYPANOSOMA CRUZI

Q: What is the name of the disease T. cruzi causes?
A: Chagas Disease, a type of myocarditis.

Q: How is trypanosoma cruzi transmitted?
A: Reduviid bugs (“kissing bug”) come in your house –> attracted to moisture so go to your eye when you are sleeping, and leaves feces (containing T. cruzi) –> you scratch your eye, and just innoculated yourself. You can also get it through eating contaminated, undercooked food.

Q: Where do you most likely find Chagas disease?
A: South America, or people who have traveled there.

Q: What are the three stages of Chagas Disease? What are the symptoms of each stage?
A:
1. Primary Lesion — organism goes into EYE –> Romana’s Sign (body’s initial response) or Chagoma.
2. Acute Stage — organism travel through blood –> fatigue, coughing, wheezing, acute myocarditis. SO TREAT BEFORE ACUTE STAGE TO PREVENT MYOCARDITIS!!!
3. Chronic Stage — can’t see organism in blood anymore, but in tissue. Significant damage to HEART. Also go to ESOPHAGUS, delaying impulses to muscular tissue there so difficulty swallowing (megaesophagus), and COLON, causing megacolon and constipation. ALL are infections of the muscular tissue of HOLLOW ORGANS.

Q: What is the best way to diagnose Chagas?
A: microscopy — look for trypanosomes

Q: How do you treat Chagas Disease?
A: Nifurtimox, but it has limited effectiveness.

PERICARDITIS

Q: What is Pericarditis?
A: cant’ pump efficiently, fluid builds up (so can hear rubbing sounds) –> increase pressure in heart, squeezing it, hard to pump blood.

Q: What are the two organisms that cause pericarditis?
A: Adenovirus, Coxsackie B

Q: Which organism can cause both pericarditis and myocarditis AT THE SAME TIME?
A: Coxsackie B. Adenovirus can cause both pericarditis and myocarditis BUT NOT AT THE SAME TIME.

Q: How is it presented?
A: sharp chest pain, which radiates to left arm and neck, FEELS LIKE HEART ATTACK.

Q: A young person (age 20-50) develop an unexplained heart failure, arrhythmia, or symptoms of heart attack. The pain intensifies when they lay down or take a deep breath. It’s not likely to be heart attack because patient is young… what else could it be?
A: Pericarditis.

Q: What do you hear with auscultation?
A: “rubbing” sound with pericarditis rubbing against each other with the fluid there.

Q: What would u see in x-ray?
A: heart looks larger because of increased fluid in pericardium.

Q: how do you relieve pressure?
A: pericardi
ocentesis to remove fluid.

Q: Where do Coxsackie and Adenovirus enter their host cells?
A: via CAR receptors on the mucosal surface in the gut.

FEVERS OF UNKNOWN ORIGIN

Q: WHat exactly is it?
A: fevers persisting without diagnosis for at least three weeks

MONONUCLEOSIS
Q: What is?
A: fever, sore throat with swollen lymph nodes, malaise. goes away on its own.

Q: What causes mono?
A: Epstein Barr Virus, Cytomegalovirus.

EPSTEIN BARR

Q: What’s the key to EBV?
A: infects B cells, close contact, Downey cells, heterophile antibodies

Q: What are the diseases EBV cause?
A:
Mononucleosis — heterophile positive, +/- exudative pharyngitis
Burkitt’s lymphoma — Chromosome 8:14 c-myc translocation, equatorial Africa
Hairy Oral Leukoplakia — HIV patients, lytic destruction of epithelial cells
Nasopharyngeal carcinoma — epithelium of the URT — chinese, inuits

CYTOMEGALOVIRUS

Q: What is it?
A: ds linear DNA, enveloped

Q: What kinda cells does it infect?
A: infects and becomes latent in mononuclear cells (i.e. monocytes & lymphocytes)

Q: How does it transmit?
A: mucosal contact.

Q: How do you diagnose it?
A: owl’s eye inclusion, heterophile negative

Q: How do you treat CMV?
A: Ganciclovir or cidofovir

Q: What diseases can CMV cause?
A:
Heterophile negative mononucleosis — primarily in transfusion patients, no pharyngeal exudate
Cytomegalitic inclusion disease — blueberry presentation (purpura pneumonitis), jaundice, CNS damage, hepatosplenomegaly.

Q: What is the most common in utero infection in the US?
A: Cytomegalitic inclusion disease caused by CMV!!

HUMAN T-LYMPHOTROPIC VIRUS (HTLV)

Q: What is the disease?
A: It can cause leukemia as well as Tropical Spastic Paraparesis. Found in equatorial (tropical) regions

Q: How does HTLV cause neurological damage in Tropical Spastic paraparesis?
A: HTLV go to lymphocyte –> go to CNS –> cytokines in infected cells cause demyelination –> progressive weakness, paralysis

Q: How do you treat HTLV?
A: AZT + IFNalpha

MALARIA

Q: What are the four types of plasmodium that cause malaria?
A: P. vivax, P. falciparum, P. malariae, P. ovale

Q: Which one is most common cause of malaria?
A: P. vivax (80%), but not as severe as P. falciparum.

Q: Why is P. vivax less severe than P. falciparum?
A: because only infects young, immature erythrocytes (so small population of RBCs) whereas P. falciparum infects all erythrocytes.

Q: What is hypnozoite?
A: latent form of P. vivax that forms. P. falciparum does not form hypnozoites. So even though more severe, it doesn’t stay latent, so don’t hafta worry about it once you’re cured from P. falciparum.

Q: What is the infectious agent?
A: sporozoite protozoan

Q: How is malaria transmitted?
A: anopheles mosquito. if you travel around, you could get a mixed infection of both vivax and falciparum.

Q: How are you infected?
A: inject sporozoite into blood by mosquito –> go to liver –> enter hepatocyte via circumsporozoite protein (CSP) –> form merozoites (tissue schizont) in the liver cells –> rupture hepatocytes and move into circulations.

Q: How do merozoite P. vivax and P. falciparum attach to RBC?
A:
P. vivax binds to RBC Duffy antigen on the host.
P. falciparum uses its PfEMP-1 antigen on itself to bind to RBC.

Q: Once inside RBC, what does the merozoite do?
A: merozoite differentiates into ring-shaped trophozoite inside RBC –>replicates (asexual) using hemoglobin as nutrients –> released from RBC as merozoite by rupturing RBC –> some become gametocyte (sexual form) to be picked up by virus. The rest can stay as merozoite to infect other RBCs.

Q: Why is this process important?
A: Because each stage you can see clinically in a patient.

Q: What process causes the symptoms of the disease?
A: rupture of RBCs and your own immune response. Causes cyclic paroxysms of fever due to release of toxic substances. Type III hypersensitivity as well.

Q: What is the presentation of malaria?
A:
Hemolytic anemia — due to rupture of RBC.. duh
Hypoglycemia — due to liver damage
Sludging of infected RBCs (RBCs stick to each other and to walls of vessels) –> hypotension. See mainly in P. falciparum because it infects all cells (cause nobs to stick out of RBCs) whereas you may see it for P. vivax, but since it only infects a small proportion of the RBCs, you basically don’t really see the cells sticking together.

Q: What is cerebral malaria?
A: more common in children. causes coma.

Q: What are the kidney complications of malaria?
A: Seen in falciparum malaria. Kidney destruction, seen more in adults. RBC destruction –> released byproducts –> released in urine –> black urine (aka “Blackwater Fever”). Also other products of hemolysis can cause acute tubular necrosis, especially when there’s also acidosis and dehydration.

Q: How do you diagnose malaria?
A: detect trophozoites in RBC sample. Also use rapid test for P. falciparum and P. vivax.

Q: How do you treat malaria?
A: Use combination antibiotics.

BABESIA

Q: what is the infectious agent?
A: sporozoite protozoa

Q: What is the reservoir for Babesia?
A: wild animals. They are trasmitted via ticks.

Q: Where does Babesia occur the most?
A: Northeast and upper midwest US i.e. New England, New York, Wisconsin, Minnesota.

Q: What co-infection do you often see with a babesia infection?
A: Borrelia burgdoferi (which remember also carried by ticks — Lyme disease)

Q: What symptoms do you get with babesiosis?
A: First of all, most people are probably asymptomatic. But the people who do get symptoms, they get malaria-like symptoms, like fever, chills, sweating, myalgia, hepatosplenomegaly, hemolytic anemia, etc.

Q: Babesiosis may be fatal in what kinda patients?
A: asplenic patients!

Q: Which Babesia species is more fatal? Which one is less severe?
A: B. divergens is more severe (fatal if untreated), and B. microti is less severe.

Q: How do you diagnose babesia?
A: look for ring structures and “maltese cross” in the RBCs. You could also do paired sera.

Q: How do you treat babesia?
A: clindamycin + quinine

DENGUE FEVER

Q: What is the infectious agent of Dengue Fever Virus (Flaviviridae family)?
A: enveloped, ss + sense RNA, four serotypes

Q: What does Dengue affect?
A: monocytes/macrophages, B/T cells, cause apoptosis of endothelial cells

Q: What is the reservoir?
A:
monkeys
and humans. transmitted by Aedes mosquito

Q: What are the three presentations?
A: Dengue Fever, Dengue Hemorrhagic Fever (DHF), Dengue Hemorrhagic Syndrome (DHS)

Q: What is Typical uncomplicated dengue fever?
A: 1 week, fever up to 105, retro-orbital pain/frontal headache, severe joint and muscle pain in lower back, maculopapular/petechial rash. INCREASED BRUISING AND GUM BLEEDING (like when brushing teeth)

Q: What is Dengue Hemorrhagic Fever (DHF)?
A: caused by different serotype. now see bullae instead of petechial lesions. cross reacting antibodies increase the infection and activate macrophages –> cytokine storm.

Q: What is Dengue Shock Syndrome (DSS)?
A: hypovolemic shock, massive bleeding

Q: How do you diagnose DSS?
A: look for NS protein (seen in first week). NS used in replication of virus (like p24 of HIV, very early in infection). Clinical presentations.

Q: How do you treat dengue?
A: supportive treatment, supportive fluid, stay away anything that thins the blood.

Q: How do you prevent?
A: vector control, like using mosquito food (blocks larval stages), there is a vaccine in clinical trials now (need to use all 4 serotype) so the vaccine is tetravalent.

Q: What regions have Dengue?
A: Tropical regions.

Q: Is it a lifelong infection?
A: NO! most lifelong infections are DNA VIRUSES!! You can’t incorporate RNA into our genome.

EHRLICHIA CHAFFEENSIS

Q: What family does it belong to?
A: Rickettsia (so very very tiny)

Q: What infectious agent?
A: gram negative, INFECTS MONOCYTES (so intracellular)

Q: How is it carried?
A: via ticks (like those carried on deer, mice, dogs, etc.). But remember ticks need to be sucking on your blood for at least 12 hours or so before the bacteria transmits, because when ticks suck blood, it’s a 1-way flow. Only when they are done feeding do they regurgitate into your blood stream a little bit. So please don’t freak out when you just see a tick.

Q: What is the disease?
A: Human Monocytic Ehrlichiosis rash is RARE. body aches, fever.

Q: How do you diagnose it?
A: see morulae vacuole (filled with the bacteria) inside the monocyte in a blood sample.

ANAPLASMA PHAGOCYTOPHILUM

Q: How is it similar to ehrlichia?
A: also member of rickettsia family, gram negative, and transmitted by tick. BUT INFECTS PMNS (NOT MONOCYTES)!!! like neutrophils

Q: What is the disease?
A: Human Granulocytotropic Anaplasmosis

Q: How do you diagnose?
A: Look for infected neutrophils — also has morulae filled with bacteria. decreased neutrophil count.

Q: Since anaplasma and ehrlichia look a heck a lot alike, how am I supposed to know what macrophage and neutrophil look like?
A: neutrophil has trilobed nucleus (since it is PMN), monocyte doesn’t — only 1 nucleus.

BORRELIA RECURRENTIS

Q: What is it?
A: gram negative spirochete, extracellular binds to surface of RBC, cause “rosetting“, antigenic variation –> relapsing disease

Q: Transmission:
A: human lice — occurs when lice is crushed –> spirochetes are released and penetrate skin…. sooooo don’t crush your lice?? also ticks.

Q: Cause what?
A: Relapsing Fever — goes up and down — usually 3 relapses and diminish in intensity over time. jaundice, hepatosplenomegaly.

Q: What does rosettes cause?
A: hemorrhaging, reduced capillary flow, rash (petechiae)

Q: How do you diagnose?
A: see spirochetes in blood smear during febrile periods. See rosettes in RBCs.

BRUCELLA

Q: Describe.
A: intracellular, gram negative rod

Q: What’s the transmission?
A: unpasteurized milk, soft cheeses. because reservoir is cattle, goats, sheep, pigs, dogs. You can also get it through any contact with these animals, like farmers and butchers.

Q: Virulence factor?
A: LPS (but has phase variation), prevents phagosome fusion with lysosome. Also has SOD to resist serum killing.

Q: What is good with phase variation?
A: Lets the organism hide. Keeps switching between smooth and rough phases. Smooth colonies have O chain on LPS. Rough don’t.

Q: What does Brucella infect?
A: infects macrophages and monophages.

Q: Cause what disease?
A: Undulant Fever — fever peaks every afternoon –> depressing.
Sweat a lot and it’s stinky.

Q: What is chronic brucellosis?
A: recurrent fever, joint pain, fatigue, depression.

Q: How do you diagnose?
A: Blood smear.

Q: Is there a vaccine?
A: YES, but ONLY FOR CATTLE…. NOT FOR HUMANS!!!!!!!!!!!!!!!!!!!!!!!!!!

INFECTIONS TARGETING THE VESSELS

RICKETTSIA RICKETTSII

Q: What is the infectious agent?
A: intracellular bacteria, gram negative

Q: What does it infect?
A: endothelial cells lining small arteries, veins, and capillaries.

Q: How are they transmitted?
A: ticks. highest in spring and summer.

Q: What is the disease?
A: Rocky Mountain Spotted Fever

Q: What is the Triad of RMSF?
A: Fever, Headache, Rash

Q: Describe the rash
A: vasculitis. ANKLES and WRIST first!!! (what makes it special)

Q: How do R. rickettsii and R. prowazekii exit the cell?
A: R. rickettsii exits via filopodium focal lysis of the cell. basically the actin of the cell help push it out of the cell.
R. prowazekii exits via lysis of the cell.

Q: If you dont’ treat, when will you die?
A: after 8-15 days. but before that you’ll get gangrene.

Q: Diagnosis:
A: history of tick bite, DFA skin lesion biopsy… and START TREATMENT ASAP before lab confirmation!!!!!!!!!!!

Q: Where do you find RR?
A: despite it’s name, it’s not really found much in the Rocky Mountains. Instead, most cases are in the South.

RICKETTSIA PROWAZEKII

Q: What is it?
A: gram negative, obligate intracellular

Q: transmission?
A: mice, squirrels carrying feces of human body lice.

Q: What does it infect?
A: endothelial cells of blood vessels.

Q: Disease?
A:
Epidemic Typhus (“camp fever” or “louse-bourne typhus”)
Brill-Zinsser Disease — which is a milder form of epidemic typhus that recurs after a latent period.

Q: Describe the rash:
A: BEGINS ON CHEST about five days after fever –> go to trunk and extremities. Becomes petechial. Your blood pressure falls.

Q: So compare Rickettsia Rickettsii with Rickettsia Prowazekii:
A:
R. Rickettsii — tick — pushed out by actin — wrist and ankle rash — rocky mountain spotted fever
R. Prowazekii — lice — lyses cell to exit — chest rash — epidemic typhus

EBOLA

Q: infectious agent
A: enveloped, ssRNA

Q: What does it infect?
A: endothelial lining vasculature, and also neutrophils.

Q: What is the reservoir?
A: wild monkeys — Zaire, Sudan, Congo, Gabon, Cote d’Ivoire

Q: Disease:
A: Ebola/Hemorrhagic Fever

Q: Describe the Rash.
A: raised rash –> viral replication –> breakdown of endothelial cells –> vascular injury and necrosis in liver, spleen, lymph nodes, and lungs –> bleeding from mucous membranes.

Q: Diagnosis:
A: ELISA and PCR to confirm. Level 4 handling.

Q: What do you do to patient?
A: QUARANTINE THEM!!!

CHIKUNGUNYA VIRUS

Q: infectious agent:
A: enveloped, +ssRNA

Q: What does it infect?
A: endothelial cells –> rash

Q: What is the reservoir?
A: Humans and Monkeys

Q: How is it transmitted?
A: Aedes Mosquitos

Q: disease?
A: Chikungunya fever (“Saddleback fever“) — flu-like symptoms, prolonged fatigue, recurring. joint edema and pain — hence the name means “bend over”, because joints so painful want to bend over. Rash can also occur due to leakage of RBCs after endothelial cells destroyed.

Q: Where do you see it?
A: India, Reunion island, Italy — spread by mosquitos

Q: Very similar to Dengue. How can you tell difference?
A: Use PCR. an IgM capture ELISA.

Q: How bad is this virus?
A: it’s self-limiting, cure on its own within 3-5 days, but you could have joint pain for months.

LASSA VIRUS

Q: Infectious agent:
A: Enveloped negative ss RNA, SEGMENTED!!

Q: What does it infect?
A: endothelial cells, dendritic cells, macrophages, lymphoid organs, liver, CNS, etc.

Q: Reservoir?
A: Mastomys Rat in West Africa.

Q: Transmission?
A: urine/feces of rodents. also transplacental.

Q: Disease?
A: Lassa Hemorrhagic Feverendothelial cell damage/ capillary leak, can get deafness, swollen baby syndrome

Q: How do you diagnose?
A: ELISA (detect Lassa antigen)

Q: How do you treat?
A: Ribavirin — give early. Otherwise just give supportive care.

Q: How bad is it?
A: first of all, 80% ppl who get it are assymptomatic. It can be fatally severe though, especially if you are a pregnant woman or a fetus.

WUCHERERIA BANCROFTI/BRUGIA MALAYI

Q: What kind of organism is it?
A: Nematode (Filarial nematode).

Q: What is the larval stage known as?
A: Microfilariae

Q: Transmission?
A: Mosquitos –> injects larval form in blood stream –> years in bloodstream before see symptoms.

Q: What time of day do the filaria come out?
A: Deep veins during the day and come out to play at night. Get blood sample at night!

Q: Where?
A: Tropics

Q: What does it cause?
A: Elephantism — filaria obstructs lymph –> lymph backs up –> edema of lower regions in body

Q: Clinical disease:
A: Lymphatic Filariasis aka Elephantiasis aka Bancroftian Filariasis

Q: What are the two phases?
A: Asymptomatic phase — occur for years. humoral response. filaria in blood for years and grow up.
Inflammatory Phase — worms disrupt flow of lymph & antigens from female adult worm cause inflammatory response –> lymphedema, fever, chills, orchitis, epididymitis.
Obstructive Phase (Chronic) — lymph varices, lymph scrotum, lymph in urine (chyluria) — basically lymph everywhere –> elephantiasis, scarring. No more microfilaria in blood.

Q: Diagnosis?
A: Look for microfilaria and eosinophilia (which attacks helminths) in blood smear. Antigen capture ELISA

Q: best protection:
A: VECTOR CONTROL!! getting rid of mosquitos

GASTROINTESTINAL BUGS

Q: How are majority GI bugs transmitted?
A: Fecal-Oral route

Q: What are the primary defense mechanisms of the GI tract against bugs/
A: Stomach — chemical barrier (i.e. gastric acidity)
Small Intestines — bile and peristalsis prevents colonization
Large Intestines — Normal Flora outcompetes the bugs.

ESOPHAGITIS

Q: What causes it?
A: Candida, HSV, CMV (also a herpes virus). They enter the GI mucosa after acid reflux.

Q: Symptoms?
A: painful/difficulty swallowing, acid reflux, heart burn.

Q: Method of diagnosis?
A: endoscopy is most common. also biopsy or xray

CANDIDA ALBICANS

Q: Clinical Disease?
A: Yellow/white mucosal plaques all along the esophagus –> Dysphagia (difficulty swallowing) and Odynophagia (painful swallowing)

Q: Treatment?
A: Fluconazole

HERPES SIMPLEX VIRUS

Q: Both HSV and CMV cause what?
A: Ulcer-like lesions in esophagus.

Q: What is unique about HSV’s ulcers?
A: In HSV, the ulcers are grouped together (multiple), and look like volcanos (raised edges with crater)

Q: Treatment?
A: Acyclovir

CYTOMEGALOVIRUS

Q: Transmission?
A: body fluids, close contact

Q: Risk population?
A: AIDS patients

Q: Symptoms?
A: Large and shallow “punched-out” ulcers in esophagus

Q: Treatment?
A: Gancyclovir

INTOXICATION/TOXICOINFECTIONS

Q: What are signs and symptoms?
A: vomiting (toxin), diarrhea (toxin), dysentery/inflammatory diarrhea (from invasive organism)

Q: What is the definition of diarrhea?
A: 3 or more loose stools within 24 hr period.

Q: What are the bugs that cause diarrhea?
A: Staph aureus, Bacillus cereus, Clostridium perfringens, Clostridium botulinum

STAPH AUREUS

Q: What are the virulence factors?
A: Produce 5 different enterotoxins!! Remember, gram positive, catalase and coagulase positive.

Q: How do you get it?
A: eating contaminated foods, primarily creamy foods like mayonnaise, custards, etc. Most of the food poisoning you get will probably be from staph aureus. A dose as little as 1 ug of toxin can get you sick.

Q: How does staph make you vomit?
A: It has toxins that stimulate vagus nerve endings in the stomach that cause you to vomit. The toxins are also superantigens that stimulate T cell proliferation (which release TNFα and IFNγ into blood stream).

Q: If you microwave or cook infected food, would that stop you from getting diarrhea and vomiting and stuff?
A: No, because all you did was kill the organism, not the toxin, which is heat-stable.

Q: How long after you ingest the staph aureus toxin do you get symptoms (vomit, diarrhea, nausea)?
A: RAPID ONSET… 1-6 hrs.

Q: When does it self-resolve?
A: 24-48 hours!!! so takes a whole day or two to recover.. which really sucks.

BACILLUS CEREUS

Q: What is it?
A: Gram positive, spore-former. beta-hemolytic.

Q: What kinda foods do you see more bacillus cereus?
A: Root vegetables (remember staph aureus = creamy foods, like potato salad)

Q: What are two types of food poisoning syndromes you can get with bacillus cereus?
A: Emetic Intoxication — RAPID ONSET (1-6 hrs incubation) — Cereulide toxin (HEAT STABLE) — stimulates vagus nerve. VOMITING. boiled RICE, fried rice, pasta, etc.
Diarrheal Intoxication — SLOW ONSET (6-16 hrs incubation) — HEAT LABILE toxin — stimulat
es adenylate cyclose. WATERY DIARRHEA. meats, stews, gravies, milk, etc. (compare this with staph aureus which also cause diarrhea but rapid onset)

CLOSTRIDIUM PERFRINGENS

Q: Infectious Agent?
A: Gram positive, spore-former (like bacillus cereus). anaerobe, but aerotolerant.

Q: Virulence factor?
A: HEAT LABILE enterotoxin

Q: High risk foods?
A: Meat products

Q: How do you prevent?
A: Since the toxin is heat labile (meaning it can be killed by heat), all u hafta do is just reheat the food or refrigerate it.

CLOSTRIDIUM BOTULINUM

Q: Infectious Agent?
A: Gram positive, SPORE FORMING bacilli, OBLIGATE ANAEROBE

Q: Virulence Factor?
A: Botulism toxin (HEAT LABILE)

Q: Reservoir?
A: Soil, normal flora

Q: Transmission?
A: foods contaminated with spores, food that’s been out (like in warm oven). Improperly canned food.

Q: What kinda toxin is Botulinum toxin?
A: AB toxin — lets it endocytose into neuron cell.

Q: What does it cause?
A: Flaccid paralysis (prevents release of acetylcholine)

Q: What happens in food-bourne botulism?
A: 12-72 hrs incubation period –> bilateral descending paralysis,dry mouth, dilated fixed pupil, diarrhea –> may take months to years to recover

Q: What is infant botulism?
A: 3-30 days incubation. floppy baby syndrome.

Q: What foods can babies get infant botulism?
A: honey

Q: What is wound botulism?
A: instead of eating the spores, the spores land in your wound, and contaminates it.

DIARRHEAL DISEASE

NON-INFLAMMATORY DIARRHEA

Which acute diarrheal disease causes the most deaths?
A: Rotavirus.

ESCHERICHIA COLI

Q: What is the infectious agent?
A: gram negative, lactose fermenting, indole positive.

Q: What are the Adhesins and exotoxins?
A: Adhesins: CFA, Bfp, AAF
Exotoxin: Sta (allow cGMP to increase), STx (allow cAMP to increase), LT –> watery stools

Q: Clinical Disease?
A: Traveler’s Diarrhea: ETEC (enterotoxigenic)
Childhood Diarrhea: EPEC (enteropathogenic), EAEC (enteroaggregative)

Q: where does it colonize?
A: Small intestines

Q: What is ETEC?
A: Enterotoxigenic E. Coli — incubation for 1-3 days, then watery diarrhea 3-7 days

Q: WHat are the virulence factors?
A: Heat-labile toxin (LT) (CHOLERA-LIKE TOXIN) and Heat-stable toxin a (STa)

Q: What is EAEC?
A: Enteroaggregative E. coli — infantile diarrhea in under-developed countries, produce ST-like toxin (called EAST1), altered calcium rather than chloride (influx of calcium), shortening of microvilli, see stacked bricks (autoagglutination of bacteria) –> biofilm on intestines –> watery and oily stool — blocks reabsorption of water.

Q: What is EPEC?
A: Enteropathogenic E. Coli — infantile diarrhea — no LT or STa etc.

Q: How does EPEC get in?
A: EPEC adheres via Bfp –> injects Tir into the cell –> intimin binding –> rearanges the actin –> forms pedestal –> loss of absorptive barrier (destruction of the microvilli) –> malabsorption –> diarrhea

VIBRIO CHOLERAE

Q: Infectious agent:
A: curved-shaped bacilli, monotrichous flagella found in salt water, more than 200 types of serotypes

Q: Transmission?
A: improperly cooked seafood, salt water

Q: What’s the clinical disease of Vibrio infection?
A: Cholera!!!!!!!! rice water stools (colorless feces because so much water, some mucus) — u could die from dehydration. You could also get loss of skin elasticity because of dehydration.

Q: What virulence factors do vibrio have?
A: cholera toxin (duh), Toxin-co-regulated pilus (TCP) — but these are only in O1 and O139 strains.
Hemagglutination protease, Neuraminidase, Pili/Adhesins.

Q: How do you diagnose cholera?
A: culture in thiosulfate citrate bile salt agar (TCBS agar)

Q: How do you treat?
A: rehydration!!

Q: Is there a vaccine?
A: yes, it is a killed, whole cell.. but not very life-long.. need 6 month boosters — good for tourists who aren’t going to stay somewhere very long.

Q: What are the other types of Vibrio?
A: V. parahemolyticus — self-limiting diarrhea
V. vulnificus — necrotizing fasciitis in immunocompromised patients.

LISTERIA MONOCYTOGENES

Q: What is it?
A: facultative intracellular gram + bacillus, non-spore-former.

Q: Reservoir?
A: from soil.

Q: Transmission?
A: Fecal-Oral, with a high infectious dose.

Q: Disease?
A: Listeriosis

Q: Virulence factors?
A: Act A, Internalins, Listeriolysin, and PLC

Q: How do u diagnose?
A: PALCAM agar — forms black halo (due to esculin hydrolysis) AND does not ferment mannitol.

7/22/2010 (and 7/23/2010 was a review day)

GIARDIA

Q: What does Giardia look like?
A: looks like a kite! It is a protozoan. has lots of flagella, 2 nuclei. attaches to mucosa of duodenum via a ventral sucking disk.

Q: Reservoir?
A: beavers, cattle, dogs, cats, etc.

Q: Transmission?
A: Oral-fecal, contaminated food and water (like drinking from pond)

Q: Risky places to get giardia:
A: Daycares, prisons, homeless

Q: What is the most common parasitic intestinal disease in the US?
A: GIARDIA!!

Q: What is the disease?
A: Giardiasis — foul smelling, watery diarrhea (but really, what diarrhea ISN’T foul smelling?). FLATULENCE!! NO blood, mucus or leukocytes in stool.

Q: How do you diagnose Giardia?
A: find TROPHOZOITE or CYST in stool.

Q: Why do you need thre
e stool specimens to diagnose Giardia?
A: Because Giardia isn’t always present in the stool… it only comes all at once, once in a while.

Q: Can you kill the cyst with drugs?
A: NO, you can’t even kill cyst with chlorinated water, but you can boil or filter water. you can target the trophozoite with drugs.

Q: How do you treat Giardia?
A: target the trophozoite — use Quinacrine, Metronidazole

CRYPTOSPORIDIUM PARVUM

Q: Infectious agent?
A: Sporozoan, intracellular

Q: Can chlorination kill cryptosporidium?
A: NO

Q: Transmission?
A: Oral-fecal, contaminated food and water.

Q: Risk factors:
A: immunocompromised

Q: Clinical Disease?
A: Cryptosporidiosis, AIDS-associated diarrhea.

Q: What form of cryptosporidium do you ingest?
A: Oocyst

Q: What is in each cryptosporidium oocyst?
A: Has 4 sporozoites.

Q: Which form parasitizes the intestinal epithelial cells?
A: Sporozoites –> asexual and sexual reproduction.

Q: What is the male cryptosporidium? what is the female?
A: Male = microgamonts. Female = macrogamonts

Q: Which form exits the host via the feces?
A: Oocyst (so oocyst is the form that both enter and exit the host)

Q: How do you diagnose Cryptosporidium?
A: find oocyst in stool. acid fast stain.

Q: how do you treat?
A: self-limiting. Remember the disease is mainly in immunocompromised patients.

CYCLOSPORA CAYETANESIS

Q: How long does it take for cyclospora to actually cause infection?
A: Days to weeks.

Q: Transmission?
A: contaminated water, foods. GUATEMALAN RASPBERRIES.

Q: Disease?
A: Cyclosporiasis — onset after 7 days.

Q: Can you get cyclospora directly from eating fecal matter?
A: NO! because the cyclospora that comes out of feces is NOT infective (because it is UNSPORULATED). It needs to be in the environment for days/weeks at medium temperatures for it to sporulate (and become infective).

Q: Cryptosporidium oocyst and cyclospora oocyst look aweful a lot alike… how do you tell the difference under a microscope?
A: Cyclospora have larger cyst, and they autofluoresce.

Q: How do you treat cyclospora?
A: self-limiting.

ISOSPORA

Q: What is it?
A: Sporozoan protozoan

Q: Reservoir?
A: Humans only.

Q: Where?
A: tropics.

Q: Transmission?
A: ingestion of oocyst in contaminated food/water.

Q: Risk populations?
A: Immunocompromised people.

Q: Disease?
A: Isosporiasis — AIDS-associated diarrhea, but also traveler’s diarrhea.

Q: What shape?
A: OVAL!!

Q: How is isospora like cyclospora?
A: Also autofluoresce under UV. also must be in environment for a few days (but shorter 2-3 days) in order for it to become infective (so no direct fecal-oral infection).

Q: How do you treat?
A: Trimethoprim-sulfamethoxazole

Q: So in summary, compare what the oocysts of cryptosporidium, cyclospora, and isospora look like:
A: Cryptosporidium = round — fecal/oral
Cyclospora = larger round, autofluoresce — contaminated food
Isospora = oval, autofluoresce — contaminated food

CALCIVIRIDAE NOROVIRUSES (NORWALK VIRUSES)

Q: What are these?
A: positive ssRNA, non-enveloped.

Q: Where do you get outbreaks?
A: Cruise ships, institutions.

Q: What is the most common cause of nonbacterial gastroenteritis?
A: calciviridae noroviruses!

Q: What do they look like?
A: Star of David

ROTAVIRUSES

Q: What do they look like?
A: Look like wheels, he
nce its name.

Q: Infectious agent?
A: dsRNA!!!! (SEGMENTED), non-enveloped.

Q: Can you use detergents, acids, or drying to stop it?
A: NO! resistant to all of these.

Q: Who’s at risk?
A: INFANTS AND CHILDREN!!!! In fact, it is the #1 cause of diarrhea in children.

Q: What seasons do you get it the most?
A: Winter/Spring

Q: WHat is the clinical triad of rotavirus infection?
A: Fever, Vomiting, Diarrhea.

Q: How do you diagnose?
A: Look for those wheels in the feces.

Q: What are some Rotavirus vaccines?
A: Rotashield — live, attenuated, reassortant, oral vaccine (NO LONGER RECOMMENDED, because causes intussusception bowel obstruction in infants)
RotaTeq — approved in 2006. also live and reassortant, made from bovine strain.

Q: Where do most rotavirus deaths occur?
A: India.

ADENOVIRUS 40/41

Q: What serotypes of adenovirus can cause diarrhea?
A: 40 and 41

Q: Who’s at risk?
A: Infants –> infantile diarrhea, incubate for 7-8 days and infect 8-12 days.

ASTROVIRUSES

Q: How do the stars in astroviruses differ from the stars in noroviruses?
A: Norovirus stars look like star of davids. Astrovirus stars look like solid stars.

Q: Infectious agent?
A: positive ssRNA, nonenveloped.. JUST LIKE NOROVIRUS!!

Q: What does it cause?
A: Infantile diarrhea, although can also find in adults and elderly patients.

Q: How bad is the disease?
A: acute diarrhea, but milder than rotavirus.

Q: How long does it last?
A: Incubate 3-4 days, and last less than 5 days.. so not that bad.

7/26/2010

INFLAMMATORY DIARRHEA/DYSENTERY

Q: What casues it?
A: invasive organisms, usually from large intestines.

Q: What does the diarrhea look like?
A: has PUS (white blood cell due to inflammation), and can be bloody.

Q: What is tenesmus?
A: Straining (during urination or defecating)

SHIGELLA

Q: What is it?
A: gram negative, non-spore-forming.

Q: Where do you see shigella?
A: Cruise Lines, Daycares, and ppl who do analingus

Q: It has four serotypes.. which one is the most common cause?
A: S. dysenteriae.

Q: Transmission?
A: fecal-oral, only in humans. SURVIVES STOMACH ACIDITY

Q: High risk population?
A: Primarily in CHILDREN.

Q: What are the enterotoxins of shigella?
A: ShET1 and 2 — cause watery diarrhea

Q: S. dystenteria produces what cytotoxin?
A: Shiga toxin — interupts ribosome (so inhibit protein synthesis). It is an AB toxin.

Q: What is Shiga toxin associated with?
A: HUS (hemolytic uremic syndrome) — ppl less than 10 yrs old.

Q: What’s the disease?
A: Shigellosis (Bacillary dysentery) — tenesmus (crampy rectal pain), PMNs in stool,

Q: What does Shigella invade?
A: SMALL INTESTINES

Q: How do you treat it?
A: Self-limiting.

Q: How do you diagnose it?
A: Green colonies, no black center, no fermentation… see all
this on Hektoen agar.

Q: If you have a patient with shigellosis, what do you have to do?
A: REPORT IT TO THE GOVERNMENT!! because shigellosis spreads easily.

Q: What are Shigella associated sequelae
A: HUS (hemolytic uremic syndrome), and Reiter’s Syndrome — HLA-B27 association

ESCHERICHIA COLI

Q: What are two agents?
A: EIEC — Enteroinvasive E Coli
EHEC — Enterohemorrhagic E Coli

Q: What do they invade?
A: LARGE INTESTINES

EIEC

Q: Where is it found?
A: Undeveloped countries

Q: What does it do?
A: Invade colonic epithelial cells and therefore produces shigella-like disease because of this. Does not have Shiga-like toxin (vs. EHEC)

EHEC

Q: WHere is it found?
A: All countries (including developed countries)

Q: What’s the disease?
A: Hemmorrhagic colitis

Q: EHEC can lead to what sequellae?
A: HUS!! can kill.

Q: What toxin?
A: Verotoxin (shiga-like toxin) — disrupts protein synthesis — destroys Vero cells.

Q: How do you differentiate from other E Coli?
A: Does not ferment sorbitol on SMAC

Q: Summarize the Five categories of E coli?
A:
ETEC (enterotoxigenic) — 小腸 — Traveller’s Diarrhea — LT (labile toxin), STa (stabile toxin) — hypersecretion of fluids
EAEC (enteroaggregative) — 小腸 — Infant Diarrhea in Developing countries — Enteroaggregative heat stable toxin — inhibition of fluid absorbtion by aggregating on surface
EPEC (enteropathogenic) — 小腸 — Infant Diarrhea — adherence to enterocytes
EHEC (enterohemorrhagic) — 大腸– Hemmorrhagic colitis — Shiga-like toxin — disrupts protein synthesis
EIEC (enteroinvasive) — 大腸 — Shigellosis-like disease — NO shiga-like toxin — invasion of enterocytes

NON-TYPHOIDAL SALMONELLA

Q: What is it?
A: gram negative, non-lactose fermenter, no capsule, PRODUCES H2S!! (so therefore has black center in the green colony on the Hektoen plate.

Q: Transmission?
A: fecal-oral, POULTRY, EGGS, Reptile pets –> INVADES epithelial cells.

Q: Salmonellosis?
A: nausea, vomiting, nonbloody diarrhea, etc.

Q: How do you diagnose?
A: green colonies WITH BLACK CENTER on Hektoen plate.

Q: Should you treat with antibiotics?
A: no — contraindicated, they do not shorten duration of illness.

Q: WHere is it found?
A: Underdeveloped countries

Q: What kinda vaccine?
A: non-typhoidal vaccine

7/27/2010

CAMPYLOBACTER JEJUNI

Q: Infectious agent?
A: Gram negative, comma or S-SHAPED rod

Q: Reservoir?
A: Poultry, pets (like goats, etc.)

Q: Risk population?
A: Young children, immunocompromised patients, people taking ANTACIDS (or anything that neutralizes the pH in the stomach)!!

Q: Clinical disease?
A: Campylobacteriosis — invasion of epithelium. not only is it invasive but it also produce cholera-like enterotoxin. TEN OR MORE STOOLS A DAY… very unpleasant!!!

Q: How do you diagnose?
A: use CAMP test. It is CAMP positive. “CAMPylobacter is CAMP positive”

YERSINIA ENTEROCOLITICA

Q: Infectious agent?
A: Gram negative rod

Q: Reservoir?
A: Animals

Q: Disease?
A: Gastroenteritis 1-10 days incubation period. Does MESENTERIC LYMPHADENITIS, which MIMICS APPENDICITIS!!! This is because it gets into the blood stream.

Q: Who gets it?
4A: Mainly in children

Q: How do you get it?
A: BLOOD TRANSFUSION, fecal oral, contaminated foods.

Q: What temperature is necessary for infective growth?
A: 4°C

Q: Treatment?
A: self-limiting

Q: What sequelae can happen?
A: reactive arthritis.

ENTAMOEBA HISTOLYTICA

Q: Infectious agent?
A: amoeboid protozoa, 2-stage life cycle

Q: Reservoir?
A: COCKROACH, flies, water, fruit

Q: Transmission?
A: fecal-oral, contaminated food.

Q: Risk?
A: anyone may get it, but emerging problem in MSM population.

Q: Disease?
A: Amoebic dysentery (aboebiasis) — last months to years. flask-shaped lesions in large intestine walls, form abscess, Right Upper Quadrant (RUQ) pain.

Q: HOw do you diagnose?
A: find cyst or motile trophozoite in feces.

Q: Treat?
A: antibiotics to reduce intestinal flora (metronidazole)

CLOSTRIDIUM DIFFICILE

Q: Infectious agent?
A: Strict ANAEROBE, spore former, RESISTANT TO STOMACH ACIDITY!

Q: Transmission via what?
A: via SPORES

Q: What are the two toxins that are produced?
A: Enterotoxin (Toxin A) — an AB toxin — attracts neutrophils, produce cytokine, hypersecretion of fluid, hemorrhagic necrosis
Cytotoxin (Toxin B) — an AB toxin — depolymerization of actin, loss of cytoskeleton.

Q: Disease?
A:
Antibiotic Associated Diarrhea — basically u take antibiotics, and it disrupts normal flora. C. difficile outcompetes them and takes over.
Clostridium Difficile Colitis — aka PSEUDOMEMBRANOUS COLITIS (pathognomonic) —
pseudomembrane casued by leukocytic infiltrate+fibrin+mucus –> YELLOW PATCHES ON MUCOSA

7/28/2010

ENTERIC FEVER

SALMONELLA TYPHI

Q: infectious agent?
A: Gram negative, lactose nonfermentor

Q: Reservoir?
A: Human

Q: Risk factors?
A: pediatric, geriatric, AIDS, traveler to endemic area

Q: Disease?
A: Enteric fever/Typhoid fever. SPLIT PEA STOOL (looks kinda greenish)!!

Q: What is the fever like?
A: prolonged fever, sustained bacteremia NO ENDOCARDIAL INVOLVEMENT. CONSTIPATION!! ROSE SPOTS ON ABDOMEN

Q: Diagnosis?
A: Widal Test — for agglutinating antibodies to flagellar (H angen) and somatic (O antigen) antigens.

Q: How do you contract typhoid fever?
A: eat contaminated food/water –> incubate –> bacteria enter mucosa cells in small intestines –> enter lymphatics –> blood stream –> go to liver/spleen –> hepatosplenomegaly –> fevers, chills, rose spots on abdomen –> gallbladder –< bile in intestines –> SEVERE ULCERS in intestinal mucosa –> could be fatal.

Q: Vaccines?
A: dead whole cells, live attenuated (strain can’t metabolize galactose)

INTESTINAL PARASITES

DIPHYLLOBOTHRIUM LATUM

Q: Proglottids.. what are they?
A: Segments of the tape worm that have both male and female parts so they can fertilize themselves… can produce up to 30,000 eggs!! You see proglottids in the stool if you are infected.

Q: What is the common name of Diphyllobothrium latum?
A: Fish tapeworm

Q: What organism is it found?
A: Freshwater fish. So cook your freshwater fish well.

Q: Disease?
A: Diphyllobothriasis — diarrhea, B12 DEFICIENCY (MEGALOBLASTIC ANEMIA)

Q: Diagnose?
A: Look for proglottids and eggs in the stool.

Q: Treatment?
A: Niclosamide, praziquantel.

TAENIA SAGINATA & TAENIA SOLIUM

Q: Common names?
A:
Taenia Saginata = Beef Tapework
Taenia Solium = Pork Tapework

Q: Transmission?
A: Ingestion of undercooked meat with larvae IN THE MUSCLE TISSUE.

Q: How big can these worms get?
A: Up to 15 feet!!

Q: What is autoinnoculation?
A: you can autoinnoculate yourself with a different stage of the organism so that instead of just being a worm in your intestines, it gets into your muscles.

Q: Diagnosis?
A: See proglottids in stool. scolex.

Q: Treat?
A: niclosamide

CLONORCHIS SINENSIS

Q: Common name?
A: Oriental Liver fluke

Q: Infectious agent?
A: Trematode

Q: What reservoir?
A: Snail (intermediate host) –> Fish/Crayfish/Crabs –> Humans (via ingestion)

Q: Disease?
A: organism go to biliary ducts of liver. liver triggers inflammatory response against organism. Cause damage to liver, biliary ducts, fibrosis and hyperplasia.

Q: Why does the organism go to the liver?
A: Because it feeds on bile.

Q: Treat?
A: Praziquantel, albendazole

SCHISTOSOMA

Q: Common name?
A: Blood Fluke

Q: Infectious agent?
A: Trematode.

Q: What’s so cool about the blood fluke’s immune defenses?
A: They coat themseves with “self” so chronic infections for 20 to 30 years.

Q: Reservoir?
A: Water –> snails –> water –> humans (NO FISH INTERMEDIATE LIKE CLONORCHIS)

Q: How do they transmit? Do you eat it?
A: The cercariae (looks like hook) penetrate the skin directly, like when you are swimming.

Q: Disease?
A: Schistosoma haematobium — primary sites of infection are veins of urinary bladder –> hematuria
S. mansoni and S. japonicum — infects GI tract — GI bleeding, diarrhea, liver damage.

Q: So if a patient comes in with hematuria, but bacterial labs come out negative. He went swimming in a lake recently.. what could he have?
A: Schistosoma haematobium.

Q: Where does the Schistosoma mansoni and Schistosoma japonicum infect?
A: GI Tract (S. hematobium infects bladder)

Q: What do non-human schistosoma cause?
A: Swimmers Itch. pathogens only dig into skin, but can’t invade.

Q: Diagnosis?
A: S. Haemotobium — terminal spine
S. mansoni — large lateral spine
S. japonicum — small lateral spine

Q: Treatment?
A: praziquantel.

7/29/2010

ENTEROBIUS VERMICULARIS

Q: What is the common name for enterobius vermicularis?
A: Pinworm

Q: Infectious Agent?
A: Nematode

Q: Reservoir?
A: HUMANS

Q: Transmission?
A: Fecal-oral

Q: Risk populations?
A: Cold climates.

Q: Disease?
A: you get a severe type IV immune response against female and eggs. Your anus can itch a lot. Worm can also enter apperndix.

Q: How do you diagnose it?
A: use scotch tape to recover female and eggs as it comes out of anus to lay eggs.

Q: How do you treat once you find out one person in the group has it?
A: Treat entire group! (so treat entire daycare or family, because eggs are laid outside)

TRICHURIS TRICHIURA

Q: Common name?
A: Whipworm

Q: Infectious agent?
A: nematode

Q:Reservoir?
A: human

Q: Transmitted?
A: ingestion of egg

Q: Disease?
A: usually asymptomatic… but sometimes abdominal pain, diarrhea, or RECTAL PROLAPSE!

Q: Diagnosis?
A: egg in stool. has a barrel shape.

Q: Treat?
A: mebendazole

ANCYCLOSTOMA DUODENALE

Q: Common name?
A: Hookworm

Q: Infectious agent?
A: Nematode

Q: Reservoir?
A: humans, cats, dogs

Q: Transmission?
A: skin penetration by larvae in soil

Q: Disease?
A: abdominal pain, ANEMIA, because of chronic intestinal blood loss.

Q: Diagnosis?
A: egg in stool

Q: Treat?
A: Mebendazole or Pyrantel Pamoate

Q: Distinguishing physical feature?
A: Chitinous Teeth (this is how it can penetrate you!)

Q: So in summary of all the worms, which treatments go with which worm?
A:
Tapeworms — Niclosamide
Flukes (Trematodes) — Praziquantel
Nematodes — Mebendazole

PEPTIC ULCER

HELICOBACTER PYLORI

Q: Infectious agent?
A: Gram negative, CURVED rod, CORKSCREW motility, CELL WALL HAS FATTY ACID

Q: What does it produce when in the stomach?
A: UREASE — creates alkaline environment. metabolizes AMINO ACID by FERMENTATION

Q: Reservoir?
A: Humans

Q: Risk factors?
A: people with gastritis, gastric ulcers, or duodenal ulcers.. any way the helicobacter can get into the body. use of NSAIDS also implicated for gastric ulcer.

Q: Helicobacter pylori can actually provide protection against what?
A: gastric reflux disease and adenocarcinomas of lower esophagus (because alkaline?)

Q: Virulence Factors?
A: Urease (neutralizes gastric acid, chemotactic), HEAT-SHOCK PROTEIN (HspB) (enhances urease).

Q: How does it cause disease?
A: bacteria come, lands on mucosa, secrete urease and HspB –> neutralizes mucus layer –> mucinase digest mucus layer –> gastric acid comes and destroys the mucosa.

Q: Disease?
A: Gastric Ulcer — Pain INCREASES with meals –> weight LOSS
Duodenal Ulcer — Pain DECREASES with meals –> weight GAIN

Q: Diagnosis?
A: biopsy, urease breath test (ingest radioactive urea and see if produce CO2)

Q: Treatment?
A: Triple or Quadruple therapy — 2 antibiotics + proton pump inhibitor (i.e. metronidazole, amoxicillin, prilosec, pepto-bismol)

7/30/2010 REVIEW DAY

8/2/2010

HEPATITIS

Q: What are the symptoms of hepatitis?
A: jaundice, dark urine, light-colored stool, enlarged spleen (if alcohol-induced hepatitis), headache (if drug-induced)

YELLOW FEVER VIRUS

Q: Infectious agent?
A: ss+RNA, enveloped

Q: Reservoir?
A: wild and domestic animals. Mosquitos.

Q: What are the two types of clinical presentations of yellow fever?
A:
1. Hepatitis-like syndrome — self-limiting
2. Massive GI hemorrhage — BLACK VOMIT, half of patients will die.

Q: What are the two types of Yellow Fever?
A:
Jungle Yellow Fever — in the jungle. so people who work in the forest. In South America and Africa
Urban Yellow Fever — when these people bring it into the city.

Q: Diagnosis?
A: detect antiviral IgM, viral antigen in blood, or viral RNA in blood.

Q: Vaccine?
A: live attenuated virus

LEPTOSPIRA SPECIES

Q: Infectious agent?
A: Gram negative spirochete with hooks

Q: Reservoir?
A: Animals

Q: Transmission?
A: contaminated water via animal urine, breast feeding.

Q: Virulence Factors?
A: LPS (because gram negative). ANTIGENIC VARIATION .

Q: Disease?
A: Leptospirosis — septic or leptospiremic phase –> immune or leptospiritic phase (due to circulating antibodies) — not bad at all.
Weil’s Disease — hepatic renal dysfunction –> JAUNDICE and renal failure

Q: Diagnosis?
A: See via darkfield microscopy, serology, PCR

Q: Treat?
A: Doxycycline

HEPATITIS A VIRUS

Q: Which hepatitis viruses are enterically transmitted? parenterally transmitted?
A: Enterically Transmitted: A, E
Parenterally (via skin penetration) Transmitted: B, D, G, C

Q: What family?
A: Picornaviridae

Q: Infectious agent?
A: ss+RNA, no envelope. resists acidic, dry, salty environments, but can be inactivated by chlorine.

Q: Reservoir?
A: Human

Q: Transmission?
A: fecal-oral, because excreted in feces.

Q: Disease?
A: ACUTE, self limiting — diarrhea, dark urine, vomiting AND jaundice. NO CHRONIC. (Mnemonic: A for Acute)

Q: How does hepatitis A virus spread within the body?
A: oral –> crosses intestines –> blood –> liver –> bile –> stool.

Q: Diagnosis?
A: HAV-IgM, HAV-IgG (determines past infection)

Q: Prevention?
A: If not immunocompromised — vaccination
If immunocompromised — immunoglobulin
If post-exposure — immunoglobulin

HEPATITIS E VIRUS

Q: Family?
A: Caliciviridae

Q: Infectious agent?
A: spherical, non-enveloped, ss+RNA

Q: Transmission?
A: fecally contaminated DRINKING WATER

Q: High risk population?
A: WOMEN IN THIRD TRIMESTER (high mortality)

Q: Disease?
A: ACUTE!! NO CHRONIC (mnemonic: E for Ecute)

Q: Diagnose?
A: clinically same as Hep A. serology.

8/3/2010

HEPATITIS B VIRUS

Q: Family?
A: Hepadnaviridae

Q: Infectious Agent?
A: enveloped, partially ds circular DNA (so uses RNA intermediate, but since it’s DNA, can intergrate into host genome), DANE PARTICLE (infectious)

Q: Reservoir?
A: Humans, CHIMPANZEE

Q: Transmission?
A: breast milk, transplacental, parenteral (i.e. tattoos, piercings)

Q: How bad is it?
A: Most patients will recover from it.

Q: Where does it attack?
A: liver, pancreas, kidneys

Q: Disease?
A: ACUTE AND CHRONIC (since it’s a DNA virus): (Mnemonic: B for Both chronic and acute)
1. Chronic Persistent Hepatitis — asymptomatic, but can lead to extrahepatic diseases (glomerulonephritis, etc)
2. Chronic Active Hepatitis — symptomatic
3. Cirrhosis of Liver
4. Hepatocellular Carcinoma

Q: What determines if you end up with acute, chronic, or autoimmune disease?
A: cell-mediated response or inflammatory response –> symptoms BUT resolution
ineffective T cell response –> mild symptoms BUT chronic disease
B cell response (HBsAg bind anti-HB ab) –> immune complex form –> autoimmune disease

Q:Diagnosis?
A:
HBsAg — shows infection (s = surface)
HBsAb — shows recovery
Anti-HBcIgM — shows
acute infection
Anti-HBcIgG — shows chronic infection
HBeAg — shows virus is REPLICATING — so HIGH TRANSMISSION RISK
Anti-HBe — shows virus is NOT REPLICATING — so LOW TRANSMISSION RISK
HBV-DNA — also shows virus is replicating

Q: Treatment?
A: Interferon α, LAMIVUDINE (reverse transcriptase inhibitor)

Q: Prevention?
A: Subunit vaccine.
If infant born to chronic carrier, use BOTH Ig AND vaccine!

HEPATITIS D (DELTA) VIRUS

Q: How is it different?
A: PARASITIC virus, in order for it to infect, it must pick up Hepatitis B antigen (via coinfection)

Q: Infectious agent?
A: ss circular -RNA. It acquires HBsAg coat during transmission, but NOT related to HBV (no shared DNA)

Q: Transmission?
A: piercings, needles, acupuncture, tattoo… anything that directly pierces the skin.

Q: What do you detect?
A: You detect HBsAg (which it uses for its advantage) but causes more SEVERE disease than Hep B!! You also detect Hep D antigen and Hep D antibody against it.

Q: Disease?
A: Coinfection — HDV and HBV AT SAME TIME — lead to ACUTE disease
Superinfection — when you get HDV when you already have HBV — lead to CHRONIC disease (so you see HBsAg all the time)

Q: How do you prevent?
A: prevent Hep B via Hep B vaccine (because Hep D needs Hep B to infect)

HEPATITIS C VIRUS (HCV)

Q: Family?
A: Flaviviridae

Q: Infectious agent?
A: +ss RNA, enveloped

Q: Reservoir?
A: Humans and Chimps (like Hep B)

Q: Transmission?
A: Parenteral (remember Hep BDGC all parenterally transmitted, meaning via piercing through skin)

Q: Disease?
A: CHRONIC (acute usually leads to chronic in Hep C), like chronic hepatitis B. (Mnemonic: C for chronic)

Q: Diagnosis?
A: HCV Ab, HCV RNA, HCV ag, liver biopsy

Q: Treatment?
A: Interferon α + Ribavirin combo is best

Q: What does Interferon α do?
A: It controls the chronic infection from developing into cirrhosis or hepatocellular carcinoma.

Q: Prevention?
A: NO VACCINE YET

HEPATITIS G VIRUS

Q: Family?
A: Flaviviridae

Q: Infectious agent?
A: +ss RNA

Q: Disease?
A: Just like Hep C

SUMMARY: HEPATITIS

A — fecal/oral — acute — ss +RNA — Picornaviridae
B — parenteral — both — partially ds DNA — Hepadnaviridae
C — parenteral — chronic — ss +RNA — Flaviviridae
D — parenteral — both — ss -RNA — Deltavirus
E — fecal/oral — acute — ss +RNA — Calciviridae