Infectious diseases Flashcards Preview

IHD Part 2 306 > Infectious diseases > Flashcards

Flashcards in Infectious diseases Deck (46)
Loading flashcards...

HIV symposium: How is HIV transferred?

Sexual contact

Blood- blood contact, IVDU

Infected blood products

In utero - cross placental drugs now stop this and in birth

Breast milk


HIV symposium: What are the HIV types and strains?

HIV 1 and HIV 2
HIV 1 most common
HIV 2 less easily transmitted and less pathogenic - some drugs do not work against HIV2

HIV mutates readily- Reverse Transcriptase does not proofread
Three main groups of HIV-1:
- Main (M- pandemic trains), New (N) and Outlier (O- confined to Cameroon area), many subtypes
- Infected individuals contain a heterogeneous viral population


HIV symposium: How did HIV-1 start?

The most commonly accepted theory is that of the 'hunter'. In this scenario, SIVcpz was transferred to humans as a result of chimps being killed and eaten, or their blood getting into cuts or wounds on people in the course of hunting.5 Normally, the hunter's body would have fought off SIV, but on a few occasions the virus adapted itself within its new human host and became HIV-1.


HIV symposium: How did HIV-2 start?

HIV-2 comes from SIVsmm in sooty mangabey monkeys rather than chimpanzees.7 The crossover to humans is believed to have happened in a similar way (through the butchering and consumption of monkey meat).

It is far rarer, and less infectious than HIV-1. As a result, it infects far fewer people, and is mainly found in a few countries in West Africa like Mali, Mauritania, Nigeria and Sierra Leone


HIV symposium: What are the main features of HIV virus?

adhesions on the outside of the virus - gps 120-41 which binds to the cell receptor

lipid coat the virion - enveloped - actually makes it less resistant to survival outside host

ssRNA - has RNA and RT enzyme to convert RAN to DNA

also has p24gag protein - target for HIV tests (major structural core protein)


HIV symposium: What cells does hIV infect?

CD4 CELLS - include T cells, macrophages means viral load increase can be triggered by 2’ infections and actually promoted by humoral response to HIV and dendritic cells- aid dissemination since they act as a reservoir for virus move slowly round the body and stimulate cvells in plymph nodes to produce ,,, this helps infection and dissemination


HIV symposium: How does hIV initially bind to cd4 CELLSs?

Initial attachment via gp120 binding to CD4

followed by co-receptor binding

membrane fusion and internalisation - gp41 dependent which released both the viral mRNA and RT and integrate enzymes

this then converts RNA to DNA in nucleus and then integrates into the chromosome - retrovirus

When cells are activated viral proteins are produced
And thousands of new virus progeny synthesized


HIV symposium: Which people are resistant to HIV?

People with CCR5 mutations are resistant
Occurs in 2-14% europeans (caucasian) , and 15% of Icelandic


HIV symposium: How does the virus vary during HIV infection?

Isolates from early in infection- CCR5 (M)
macrophage tropic and low cytopathic effect- more transmissable

Isolates from late infection- CXCR4 (T)
high cytopathic ability – less transmissable

i.e. at start good at transmission and finding macrophage and cd4 cells, to aid dissemination and get established in the body, but over time isolates from same person become more pathogenic and less transmissable in the progression to AIDS


HIV symposium: What are the symptoms of primary infection?

tnsient glandular fever like illness, malaise, muscle pain, throat pain, rash,

High plasma hiv levels, and transient cd4 cell depletion. Then antibodies build up and cd4 levels partially recover.

Cd4 cell continue to deplete while viral load remains largely unchaned until cd4 levels get too low

Later constitutiuonal symptoms such as diarrhoea, fevers, night sweats, weight loss. And minor infections usually of mucous membranes- candidosis, shingles, herpes. lymphomas

These often signal the onset of serious AIDS, more opp inf and tumours start

Such as kaposis sarcoma, b cell lymphomas- brain, and encephalitis- casued by release of neurotoxins by macrophages that are infected by the virus

Pneumonia is common, pneumocystis infection often diagnostic of AIDS full blown. TB, fungal- aspergillus, cyrptosporid, toxoplasmosis, cyrptococcus, oral hairy leukoplakia


HIV symposium: What opportunistic infections can you get in AIDS?

- Mycobacterium tuberculosis
- Salmonella
- Haemophilus, Streptococcus, Pneumococcus- Pyogenic infections (pus formers)- recurrent

- Cryptosporidum (chronic diaarhoea)
- Toxoplasma gondii (disseminated, including CNS- from Cats)

- Aspergillus - pneumonia
- Candida- oral presentation
- Cryptococcus neoformans- CNS
- Pneumocystis jiroveci/ carinii- pneumonia

- HSV- Herpes simplex virus- chronic oral infection
- EBV- Hairy leukoplakia, and B- cell lymphomas
- HHV-8 – Kaposis Sarcoma


HIV symposium: What are some oral manifestations of HIV?

gingival erythema
erythematous candidiasis
hairy leukoplakia


HIV symposium: how many people with hIV progress too AIDS?

10% of HIV-infected subjects progress within 2-3 years

5-10% are clinically asymptomatic after 10 years

Remaining subjects progress to AIDS within 10 years- DEATH

Situation drastically improved by antiretroviral therapy


HIV symposium: What drug targets are there for HIV drugs?

Fusion inhibitors

integrase inhibitors

PI (protease inhibitors)

CCR5 entry inhibitors

NNRTI (non-nucleoside reverse transcriptase inhibitor) - Nucleotide analogues cause chain termination when RT builds DNA from RNA


HIV symposium: What is the treatment for HIV?

Highly Active Anti-Retroviral Therapy

First line regimen
- 2 NRTIs (side-effects must be managed)
- e.g. zidovudine (AZT), lamivudine (3TC), emtricatabaine (FTC), stavudine (d4T)
- 1 NNRTI- inactive against HIV-2
- e.g. Efavirenz, Nevirapine

OR a Protease Inhibitor (PI) – high turnover in the body= many pills> boosted with Ritonavir to improve efficacy
- e.g.Indinavir (IDV), Fos-amprenavir (FPV)
OR an Integrase inhibitor


HIV symposium: What are the side effects of HIV drugs?

- AZT- headaches and nausea, anaemia, neutropenia
- Stavudine-lactic acidosis, lipoatrophy (loss from face and limbs – gain to neck and tummy) and peripheral neuropathy- possibly via mitochondrial toxicity
- rashes

- Stevens Johnson Syndrome: a severe disorder of mucous membranes
- teratogenecity

- lipodystrophy- fat loss from legs, fat gain-pot belly

- increasing problem
- drug-holidays- ineffective, compliance an issue also


HIV symposium: What is an alternative first line drug?

DTG or dolutegravir used with tenofovir disoproxil fumarate (NtRTI) & lamivudine (NRTI)

DTG – Integrase inhibitor, first used in 2014 btu becoming more and more widely used, in OK also.


HIV symposium: What is the dental transmission control for hIV?

VERY LOW RISK- even with risk contact only 1/300 chance of infection

Normal infectious control procedures
Sterilise instruments
Dispose of sharps
Care if blood spillage

If at risk- contact Occupational health physician for prophylactic HAART and HIV testing

If needlestick of HIV + patient>> PEP administration ASAP and within 72 hours at longest. (using this method NO NHS employee was infected (last 10y- no sero conversions – out of around 600 incidents).


HIV symposium: How is hIV tested for?

Most testing is ELISA based blood test- detects HIV antibodies in the blood.

antibody takes 6-12 weeks to develop

most reliable testing at 3 months (re-test at 6 months)

Babies may test positive from maternal antibody- PCR test.

Home test kits exist but blood test most reliable


HIV testing and clinical management: What are the problems with late diagnosis?

More likely to die
Transmission to others


HIV testing and clinical management: What are the clinical indicator diseases for adult HIV infection?

cerebral abscess
kaposi's sarcoma
non Hodgkin's lymphoma
cervical cancer
oral candidacies
hairy leukoplaia
head and neckk cancer
chronic parotitis


HIV testing and clinical management: check slide 13

slide 13


HIV testing and clinical management: What would you do if a patient said no to testing?

Address any issues raised by the patient

If patient refuses, explore why
? Incorrect beliefs re virus/testing


HIV testing and clinical management: How do you test for HIV?

Verbal consent
Send clotted blood to lab
“4th generation” test
Window period 1 month
Costs 99.9% PPV

other ways:
“Point of care” tests – finger prick, mouth swab, saliva
Antibody only tests
Antigen only tests
HIV RNA PCR – “viral load"


HIV testing and clinical management: What is Kaposi's sarcoma?

Human Herpesvirus-8
Usually linked with HIV

Spindle cells on biopsy

Needs referral to oncology
If not known HIV need to test!

rarely can have a genetic link
AIDs defining


HIV testing and clinical management: What can hairy leukoplakia be caused by?

Epstein-Barr Virus

White patchesCan’t be scraped off

Linked with HIV, smokingand immunosuppression


HIV testing and clinical management: What is HAART?

(Highly Active Anti-Retroviral Therapy)

3+ antiretroviral drugs

Act on different points in HIV replication cycleto suppress the virus


HIV testing and clinical management: Why does hIV become resistant to drugs?

1 mutation in every 2 new viruses produced
1 -10 billion new virus particles each day
1-5 billion mutations per day


HIV testing and clinical management: Why does hIV become resistant to drugs?

1 mutation in every 2 new viruses produced
1 -10 billion new virus particles each day
1-5 billion mutations per day

monotherapy - selects for resistant strain whereas triple therapy resistance chances are effectively zero - patient must adhere to this effectively or resistance will occur (missing one or two doses can cause resistance)


HIV testing and clinical management: What can affect the therapeutic levels of the HIV drug?

non adherence
drug drug interactions - Many drugs interact with antiretrovirals, and therefore cause subtherapeutic levels

check interactions