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What are the main microbes associated with STD's?

Bacterial - gonorrhea, syphilis, chlamydia
Protozoan - Trichomonas vaginalis
Arthropod - Lice, scabies
Viral - HIV, HPV, HSV


What is the most common STD in Utah, and most serious STD?

Chlamydia is most common, Syphilis is most serious.


What defines urethritis? And how do you treat it?

Visible drip from penis or WBCs seen on urethral gram stain. Usually accompanied by dysuria. The causes are nongonococcal urethritis (chlamydia, mycoplasma genitalium) or gonococcal urethritis (neiserria gonorrhoeae).
-For nongonococcal urethritis and cervicitis, use azithromycin.
-For gonococcal urethritis (gonorrhea), treat it with ceftriaxone, but you might have to use azithromycin for severe beta-lactam allergies.


What other diseases are associated with Mycoplasma genitalium?

Urethritis, cervicitis, endometritis, PID. Treat it will azithromycin as well because it is nongonococcal.


How do you diagnose gonococcal urethritis (gonorrhea)?

Might have rashes behind ear or on side of body as well as purulence coming from urethra. Do a urethral gram stain, should show gram-negative diplococci. Do a NAAT, nucleic acid amplification testing of urine or swab.


What are the complications of gonorrhea and chlamydia?

Infertility, epididymitis, PID, disseminated gonococcal infection in joints and skin, neonatal infection. Epididymitis is usually uniteral and involves whole testicle and spermatic cord. Treat with ceftriaxone, 3rd generation ceph. PID is caused by STD agents and by infection with normal GU flora like gardnerella vaginalis for GBS. Has tenderness around groin.


What is bacterial vaginosis?

Lactobacillus is replaced by anaerobes like gardnerella vaginalis, and is associated with STD's. You have clue cells with these which are anaerobic bacteria attached to cells, and this is a fishy odor, white discharge. Treat with metro.


What is Trichomonas vaginalis?

Associated with HIV transmission. Is a green and frothy discharge. Has flagella on back.


What is genital herpes?

Sores, and bumps or blisters, dysuria, vaginitis. Culture to see if HSV1 or HSV2. You can get HSV1 on genitals and vice versa, but probably won't have reoccurrence. Treat with acyclovir.


What is syphilis?

Caused by Treponema pallidum, which is a spirochete. Screen with syphilis IgG ELISA. You get chancres as a primary disease, red bumps on hands as secondary disease, and tertiary or untreated syphilis can spread to bone, brain, heart and is scary. Treat with Benzathine.


What is genital warts?

HPV. HPV6 and HPV11 cause 90% of all cases. Most go away within a year without intervention.


What is HAART and when did it start?

Highly Active AntiRetroviral Therapy. Mid 1990's.


Where did HIV arise from?

From SIV in equatorial Africa in early 20th century. SIV is from african monkeys. HIV-1 was a zoonosis from primates. Then the cutting of these monkeys led to this disease spread. Subtype B is most common type of HIV-1 in US. HIV-2 should disappear in coming decade.


What is HIV?

An enveloped retrovirus. Two copies of SS RNA contained within capsid. ENV protein on lipid membrane is only part of virus exposed, rest of virus becomes part of human cell. The virion contains three enzymes: RT, integrase, and protease. The gene of these is pol. The virus enters, then inside in the cytoplasm is does reverse transcriptase (mRNA template used to synthesize dsDNA), is now a double stranded DNA, then integrates into nucleus and becomes part of human chromosome, and is a pro-virus for inflammation. Then is assembles, buds, and releases from the cell, and matures outside.


What are the three structural genes that all retroviruses have?

1. gag
2. pol (RT, integrase, protease)
3. env


Which receptors does the virus need to get in a cell?

It must have a CD4 receptor, and either a CCR5 or CXCR4 chemokine receptor. The target cells are CD4+ T cells, DC's, and macrophages. Once you hit less than 200 CD4+ count, it is considered AIDS now. The viral load determines the rapidity of T cell decline.


Who should get tested for HIV?

Everyone aged 13-75, prego's, high risk groups. Who is at risk? injection drug users, MSM, etc.


How to diagnose HIV?

ELISA and Western blot (chronic), as well as detection of HIV antibodies (acute has viral load, has fever, malaise, lymphadenopathy, rash). HIV antibodies are detectable within 3 weeks of primary infection and remain detectable for life. You might get a false negative if within 3 weeks, but you would still have the virus so do a PCR. Pregnancy, mono, flu, autoimmune disease can all cause false positives. On the CD4 count chart, there is a huge drop, then after 5 weeks it rises halfway back up, and then slowly drops over the next 10 years to under 200. Meanwhile the HIV virus in plasma line does the exact opposite.


What is the worst type of AIDS?

C3, less than 200 CD4 count. A1 is asymptomatic with still high CD4 count above 500.


What are the main diseases associated with AIDS?

• Candidiasis$$
• Coccidiomycosis$
• Cryptococcosis$
• Cryptosporidiosis$
• Histoplasmosis$
• CMV$re@ni@s$
• Mycobacterial$infec@on$
• Pneumocys@s$
• PML$
• Toxoplasmosis$
• Salmonella
• Invasive$cervical$cancer$
• Kaposi$sarcoma$
• Lymphoma$
• HIV$was@ng$syndrome$
• HIV$encephalopathy$


What are the infectious complications in AIDS with a T cell count of 500? What about from 200-500?

500 = Acute Retroviral syndrome
200-500 =
1. Bacterial pneumonia
2. Tuberculosis
3. Herpes Zoster
4. Kaposi Sarcoma (HHV-8 alone is asymptomatic, but with Kaposi, non-tender vascular tumors, skin lungs)


What are the infectious complications in AIDS with a T cell count of less than 200?

1. Pneumocystis pneumonia
2. Progressive multifocal leukoencephalopathy (PML) (progressive neurologic deficits due to demyelination)


What are the infectious complications in AIDS with a T cell count of less than 100?

1. Disseminated herpes simplex
2. Toxoplasmosis (encephalitis, mass lesion on brain)
3. Cryptococcosis (meningitis)
4. Candidal esophagitis


What are the infectious complications in AIDS with a T cell count of less than 50?

1. Mycobacterium Avium Complex (MAC) (abdominal pain, fever, lymphadenopathy)
2. Disseminated CMV (retinitis, esophagitis, colitis)


What are the 4 steps in the viral life cycle that HIV drugs try and stop?

1. Viral entry
2. Reverse Transcription
3. Integration
4. Maturation


How do Viral Entry inhibiting drugs work with HIV?

They can prevent CCR5 binding to the cell, they can inhibit fusion of the receptor, they can be receptor antagonists, all of this so virus cannot bind to CD4 or CCR5.


How does reverse transcriptase inhibition work with HIV drugs?

These were the first antiretroviral drugs used, they are backbone of therapy and are always used and combined with others. You can either use nucleoside analogs or non-nucleoside inhibitors. Nucleoside analogs compete with cytoplasmic dNTPs to incorporate into proviral DNA chain. But they lack the 3'-OH, so the chain terminates and cannot undergo transcription. While non-nucleoside inhibitors bind near the reverse transcriptase active site and non-competitively inhibit reverse transcriptase. So these stop the virus from changing from a ssRNA into a dsDNA.


How do integrase inhibitor drugs work with HIV?

They bind to viral integrase and inhibit DNS strand transfer and the virus cannot be integrated inside the nucleus to our own chromosomes.


How do protease inhibitor drugs work with HIV?

After the virus is released form the cell, it matures and goes off somewhere else, but it needs to mature first. These drugs do not allow the virus to mature after budding from the cell. So they also block this new HIV form being cut into the right size proteins, and this prevents it from being infectious. And these are very potent and have a high barrier to resistance.


Why is there treatment failure when treating HIV with just a single drug?

The graph shows the plasma HIV relatively high at about 100,000, then once you start therapy, it drops down to about 200, but then after 20 days, it starts peaking again and goes back up to what it was at before, and even worse. This is with just using 1 drug. This rise is because we are encouraging the outgrowth of a resistance virus, every time RT is making a copy, it is making changes, and one of those changes will be enough to overcome the drug, and this takes about two weeks. This is when we use a single drug. Don’t ever do this.


When an HIV patient is pregnant, what drug class do you use?

Protease inhibitors. HAART effectively stops vertical transmission from mother to fetus.


Who gets gram negatives bugs the most with skin and soft tissue infections? What kind of patients?

Diabetics, burn victims.


Which hepatitis's are considered acute?

A and E, and they are both transferred fecal/oral. They incubate for several weeks, you get flu like symptoms, fever, myalgias, pharyngitis, jaundice, painful liver, elevations in LFTs, resolves spontaneously.


Which hepatitis virus is a DNA virus, while the rest are all RNA?

Hepatitis B, and can be both acute and chronic.


Which hepatitis virus causes only chronic?

Hepatitis C. Chronic can also caused by B and is often asymptomatic, physical exam shows liver inflammation, LFTs can be normal or elevated, and persists for years or decades.


Hepatitis A notes

Causes acute hepatitis. IgG is effective at neutralizing these viruses. Kids are usually asymptomatic. All children at 1 year of age get vaccinated. Fecal oral transmission.


Hepatitis E notes

Causes acute hepatitis that is indistinguishable from HAV. Fecal oral transmission as well.


Hepatitis B notes

Eneveloped DNA virus (only hepatitis DNA). It is smallest known human DNA virus. Has an overlapping layout that is super economical. It's surface protein is HBsAg. It's core nucleocapsid protein is HBcAg. Transmission depends on where you live, but can be perinatal, but vaccination is 95% effective. Can be parenteral, HBV is most common transmitted blood-borne virus in healthcare setting, then C, then HIV. Can be transmitted sexually. HBV can be both acute and chronic. Rate of progression inversely correlates with age from acute to chronic HBV.


What are the major complications of chronic HBV?

Membranous nephritis, aplastic anemia, cirrhosis, hepatocellular carcinoma, portal hypertension.


How do you diagnose HBV?

HBsAg is the surface protein and the serologic hallmark of infection during first 10 weeks. If you have it for 6 months or longer then you have chronic HBV. The clearance of HBsAg followed by development of HBsAb, means that you now have life-long immunity. The window period between decreased HBsAg and increased development of HBsAb can be several months. The co-existence of both means chronic carrier state. But you can get HBsAb from an infection as well as vaccination, so I have this antibody. HBeAg is a marker of replication and infectivity, and means they are doing worse with high viral loads. HBcAg is intracellular and never detected in serum, and HBcAb persists throughout infection. IgM HBcAb means acute infection so check for that. IgG HBcAb means you were infected at some time and don't know if it is right now or not. Common scenario: Someone has HBsAg negative, HBsAb positive, and IgG HBcAb positive, what would that mean? It would mean that they had a past infection, and not an infection, because you do not get HBcAb from vaccination. So they were exposed and they cleared it.


What are the two types of antivirals in treating hepatitis B? And what are their names?

1. IFN
2. Nucleoside analogs
-Tenofovir and Entecavir


Hepatitis D notes:

Defective ssRNA virus. It is a passenger virus alongside HBV. Common in IVDU, and big in mediterranean and North Africa. Can make HBV worse. Treat with IFN-alpha.


Hepatitis C notes:

RNA virus in Flavivirus family alongside yellow fever, dengue, west nile. It is bloodborne transmission. Leads to chronic in 60-80% of cases. High risk of cirrhosis and hepatocellular carcinoma.


What is the main drug for Hepatitis C? And what does it do?

Sofosbuvir. It is a HCV polymerase inhibitor.


Cytokines and TFs involved with Th1?

IFN-gamma and IL-12.
IFN-gamma and IL-12.


Cytokines and TFs involved with Th2?

IL-4, IL-5.


Cytokines and TFs involved with Th17?

IL-6, TGF-beta.
IL-6, IL-17.


Cytokines and TFs involved with Tfh?



Cytokines and TFs involved with Treg?

IL-10, TGF-beta.