Infectious Diseases Flashcards
Mechanism of C diff colitis
C difficile produces an exotoxin that induces necrosis of the superficial mucosa.
Management of CDI Colitis
Mild-mod - Metronidazole
Severe or recurrent - PO Vancomycin
Multiple recurrences - faecal transplant
Polyenes (amphotericin B)
MOA: Bind to membrane egosterol causing pore formation, potassium efflux and cell death.
A/E: Renal toxicity, infusion reactions, hypoK, hypoMag, hepatotoxicity.
Few drug interactions.
Pyrimidine Analogues (5-fluorocytosine)
MOA: Binds to cytosine permease, imported into cell, converted to fluorouracil by cytosine deaminase, inhibits nucleic acid synthesis
Indication:
Pathogenic YEASTS (cryptococcus)
A/E:
Bone marrow suppression, hepatotoxicity.
Azole Antifungals
Imidazoles: Clotrimizole, ketoconazole, miconazole.
Triazoles: fluconazole, itraconazole, voriconazole, posaconazole, isavuconazole
MOA: Inhibit the enzyme C13-Alpha-Sterol demethylase, which causes build up of sterol precursors and inhibits ergosterol synthesis (integral for cell wall?)
Indications: Varies for each azole.
- Candidiasis - fluconazole, itraconazole, voriconazole, posaconazole
- Cryptococcosis - fluconazole, itraconazole
- Invasive Aspergillosis (voriconazole, isavuconazole)
- Mucormycosis - isavuconazole
A/E:
- Hepatoxocity, QT prolongation, CYP450 inhibition
Voriconazole causes photosensitivity, reversible photpsia, and bone marrow toxicity
Echinocandins (caspofungin, micafungin, anidulafungi
MOA: Inhibit fungal cell wall polysaccharide B-1,3 glucan synthesis –> fungicidal. For aspergillus spp inhibits this at the hyphae tip which is fungistatic.
Indications:
- Invasive fungal infections (especially candida)
Well tolerated, minimal drug interactions.
Chlamydia trachomatis
Screen women <25year annually, and older women with risk factors.
Treat:
- Doxycycline 100mg BD for 7 days
OR
- Azithromycin 1g PO STAT (preferred in pregnancy)
Treat for LONGER if ANORECTAL INFECTION
Retest in 3 months after treatment.
Contact trace for 6 months
COVID-19
RNA virus
PCR Nasal swab has 70% sensitivity
Dengue Virus
Most common arthopod borne human disease, most common cause of febrile illness in travellers from Asia and South America.
Genus: Flavivirus
4 different serotypes.
Transmission: Aedes mosquito
Incubation: 3-14 days (usually 4-7). If fever starts >14 days after travel Dengue is very unlikely.
Symptoms: Fever, headache, back and extremity pain (breakbone fever)
Usually self-limiting disease.
If infected for a second time by a different serotype, at risk of “dengue hemorrhagic fever” with an untreated mortality rate of 50%
Dengue Hemorrhagic Fever
50% untreated mortality, 5% with supportive management.
Severe inflammatory response leads to leaky capillaries and extravasation of fluid.
Diagnosis:
Management:
- Fluid management to maintain organ perfusion
- Management of coagulopathy if significant bleeding - NO role for prophylactic transfusion.
- NO role for high dose steroids.
Phases of Dengue Infection:
Febrile phase
- lasts for 3-7 days with high fevers, headache, pain.
- Bloods often show thrombocytopenia, leukopenia, LFT derangement.
Critical Phase (more likely to occur with SECONDARY INFECTION, with a different serotype)
- around the time of defervescence (days 4-7), a small number of people develop a systemic vascular leak phase.
- increasing haematocrit, hypoproteinaemia, 3rd spacing of fluid (ascites pleural effusions).
- haemorrhage may occur in this phase, labs may show thrombocytopenia, prolonged PT and APTT, low fibrinogen. But it is not DIC.
Recovery Phase:
- Critical phase usually resolves over 48-72 hours.
Dengue Diagnosis:
PCR
ELISA for NS1 antigen
High titre IgM
Management of Human bite wounds:
- Do not close, allow to heal by secondary intention.
- X-ray to assess for fracture, foreign body or air in joint.
- Do not need to swab, is usually polymicrobial with aerobic and anaerobic bacteria
- Give prophylactic antibiotics with Amox/Clav
Flu Vaccine
- becomes effective 10-14 days after administration.
- 50% effectiveness against Flu A, 70% with flu B
- High dose trivalent vaccine recommended for >65 years.
Influenza in pregnancy:
- Can be vaccinated in any trimester
- Recommend treatment with neurominidase inhibitors with infected
Listeria Monocytogenes
Small, gram positive, facultative intracellular bacteria.
Ubiquitous in nature, and therefore acquired from contaminated food products (unpasteurised dairy, meats, vegetables)
Vertical transmission across the placenta or during delivery can occur.
Clinical disease:
- menigoencphalitis
- sepsis
- gastroenteritis
Patients affected are older, immunocompromised, diabetics, pregnant or new borns.
Infection in pregnancy can lead to premature birth or foetal death.
Intrinsically resistant to cephalosporins
Treatment is with penicillin.
Species of Plasmodium causing Malaria in humans
Plasmodium falciparum - risk of severe disease
Plasmodium vivax - usually milder disease, can cause recurrent disease.
Plasmodium malariae
Plasmodium ovale
Plasmodium wallikeri
Plasmodium knowlesi - can cause severe disease.
Malaria epidemiology
Transmission: Anopheles mosquito
Most common species:
- Africa (Falciparum)
- Asia/Oceana (Falciparum and Vivax)
- Americas (Vivax > Falciparum)
Malaria lifecycle
- Sporozoites are inoculated by the bite of a ANOPHELES mosquito
- Pre-erythrocytic phase is the liver which lasts for 1-2 weeks
- Erythrocytic phase with serial cycles of asexual reproduction causes increasing levels of paracitaemia.
- A subset of intra-erythrocytic paracites switch to sexual reproduction which produce male and female gametocytes which are transmitted back to the mosquito via a blood meal.
In Vivax and Ovale a some of the sporozoites lay dormant in the liver as hypnozoites and may cause relapse months or years later.
Pathogenesis of Malaria:
Symptoms occur once the paracitaemia passes a certain threshold (100 paracites per microL)
Incubation periods:
- Falciparum or knowlesi 10-14 days
- Vivax or Ovale 2-3 weeks
- Malariae >3 weeks
- But note some species of vivax can have incubation period up to 3-6 months.
Pathogenesis of Malaria:
Symptoms occur once the paracitaemia passes a certain threshold (100 paracites per microL)
Incubation periods:
- Falciparum or knowlesi 10-14 days
- Vivax or Ovale 2-3 weeks
- Malariae >3 weeks
- But note some species of vivax can have incubation period up to 3-6 months.
Falciparum is special. Erythrocytes with mature paracites sequester in small and medial blood vessels which causes endothelial dysfunction and obstruction:
- Brain - coma
- Lungs - respiratory disease
- pregnant women - placenta - foetal death
Anaemia caused by extravascular and intravascular haemolysis.
Clinical presentation of Malaria
Split into 2 disease presenations - uncomplicated or severe.
Uncomplicated:
- Non-specific symptoms - fever, headache, malaise, cough etc
Complicated - end organ dysfunction:
- Confusion, seizures
- Respiratory distress
- Bleeding
- jaundice
- Oliguria
- Shock
Lab criteria for complicated:
- Hb < 70, haemoglobinuria
- Hypoglycaemia
- Lactic acidosis
- AKI
- Asexual paracitaemia > 2%
Diagnosis of Malaria
Thick film - provide sensitivity
Thin film - provides quantification and speciation.
Rapid Diagnostic Tests (RDT) - detect antigen
NAAT - highly sensitive
Management of Severe Malaria
Severe malaria
- IV Artesunate ASAP
- Monitor paracitaemia 6-12 hourly
- Supportive care
- Give for at least 24 hours, and then can change to PO ACT once able to eat and drink
Adjunctive therapy:
- Bacteraemia is common, give IV Ceftriaxone until blood cultures negative
- Paracetamol
2nd line is quinine loading.
Management of uncomplicated malaria
Artemisinin based combination therapy (ACT) is first line (except in 1st trimester pregnancy)
- Artemisin rapidly reduces paracitaemia
- Combination drug gradually removes residual paracites.
Artemether-lumefantrine is used in Aus.
2nd line is atovaquone + proguanil
Locations with artemisinin resistance is increasing:
- Vietnam
- Cambodia,
- Thailand
- Laos
- Myanmar
Vivax and Ovale must be treated concurrently with Primaquine for 14 days to eliminate hypnozoites (exclude G6PD prior to giving primaquine)
Management of malaria in pregnancy
In 1st trimester give quinine and clindamycin.
After 12 weeks treatment with ACT as per usual guidelines.
Malaria prophylaxis
Strongly recommended for children, pregnant women, people staying for >8 weeks, high risk areas, patients with hyposplenism.
Vector avoidance
Medications:
1 - Atovaquone + proguanil
- start 1-2 days prior, continue for 7 days on return
2 - Doxycycline
- Start 1-2 days before going, continue for 4 weeks on return
- Not recommended for < 8 years old
3 - Mefloquine (once weekly dose)
- start 2-3 weeks prior, continue for 4 weeks on return
- high resistance in Greater Mekong Subregion.
Why continue for so long on return?
Doxy and Mefloquine are not effective against pre-erythrocytic phase in liver.
Complication of malaria
Delayed anaemia
hyper-reactive splenomegaly
Neurological sequale
Meloidosis
Caused by bacteria Burkholderia pseudomallei
- aerobic, gram negative bacilli
Endemic in Northern Australia
Increased cases during Wet Season, transmission from direct contact with soil.
More common in immunosuppressed
Usually presents as pneumonia
But any organ can be affected - basically causes a bacterial infection +/- abscess formation of any organ.
Diagnosis:
Culture - will grow on normal media, send cultures from everywhere.
Treatment:
Intensive phase: IV Ceftazadime or Meropenem for 14 days
Eradication phase: PO Bactrim for 3months
Methenamine hippurate
In the presense of acidiic urine < pH 5.5, hiprex is hydrolysed to form fomaldehyde and ammonia. Formaldehyde is bacteriocidal to almost all pathogens.
It is not effective with:
- urinary catheters, as urine is drained immediately
- Urea splitting bacteria such a proteus
Some evidence that it reduces recurrence rate of UTI
Best given with something to acidify the urine - ascorbic acid, cranberry juice
also avoid in renal and hepatic failure
Splenectomy Guidelines - Vaccination
Patients with asplenia or hyposplenia are at high risk of fulminant sepsis:
- Streptococcus pneumoniae (most common)
Immunisation with pneumococcal, meningococcal, Hib, and influenza vaccine recommended.
If surgical splenectomy - vaccinated at least 2 weeks pre. If emergency, vaccinate at least 1 week after.
Splenectomy Guidelines - Antibiotic prophylaxis:
Who gets antibiotic prophylaxis:
- children less than 5
- Patients who have had a splenectomy - start prophylaxis post op and continue for at least 3 years.
Consider prophylaxis in other people who have asplenia/hyposplenia with additional risk factors:
- Incomplete vaccination
- immunodeficiency
- malignancy
- immunosuppressive therapy
- previous invasive pneumococcal disease
Amoxicillin 250mg daily
Duration:
- Until age of 5
- 3 years post splenectomy
- Ongoing if previous overwhelming post-splenectomy infection or if significantly immunosuppressed.
Other management of aslpenia
Sick day management:
- If develops fever take 2g amoxicillin and then 1 gram 8 hourly while awaiting urgent medial assessment.
Fpr children use Amox+Clavulanic acid
Definition of asplenia / hyposplenia
Asplenia:
- Anatomic asplenia due to splenectomy
- Functional asplenia due to Sickle cell disease
Hyposplenia:
- Considered significant (and therefore warrants antibiotic prophylaxis and vaccination) if sickle cell disease, recurrent infection with encapsulated organisms, or evidence of hyposplenia on bloods - Howell Jolly bodies.
Encapsulated organisms are usually cleared by the spleen:
- Pneumococcus
- Hib
- Neiserria meningitidis
5 Categories of Fungi:
YEASTS (unicellular, white, asexual reproduction = budding, smooth round colonies)
- Candida
- Crytptococcus
MOULDS (Multicellular, organised into hyphae, variety of colours, reproduce by spore formation (asexual or sexual), Colonies appear fuzzy)
- Aspergillus
- Mucorales
DIMORPHIC FUNGI
- Can act as yeast or mould
- Mould in soils, form spores and can be inhaled, form capulated lesions in lungs
- Hystoplasma, Blastomyes, Coccidiodes, Sporothrix
DERMATOPHYTES:
- Collection of fungi that share the ability to metabolize and live on keratin from skin
- names after body part involved.
PNEUMOCYTIS
- originally thought to be parasite, now recognised to be fungi
Fungal Cell Wall
Phospholipid bilayer
Ergosterol
Chitin
B 1-3 Glucan
Glucans
Glycoprotein
Polyene Antifungal Spectrum
Amphotericin
MOA: binds to ergosterol and forms pores in fungal cell wall
Extremely broad spectrum against basically all species of fungi including yeast (most candida and crptoccus), mould (most aspergillus spp and mucorales, and the dimorphic fungi
Fluconazole Spectrum
Effective against candida albicans, but not other candida species.
1dt line for cryptococcus
Effective against dimorphic fungi
NOT effective:
- non albicans candida species
- Moulds - aspergillus or mucorales
Itraconazole
Not recommended for systemic infections.
Used for ABPA against aspergillus
1st line for mild mod disease with dimorphic fungi
Voriconazole
1st line against invasive aspergillus disease
Posazonazole
Mould active with activity against both aspergillus and mucorales.
Echinocandins Mechanism
Inhibit B 1,3 glucan synthesis which inhibits cell wall.
Results in cell lysis among Candida
Inhibits growth of aspergillus
Echinocandins Use
Emperic therapy in candida infections
Second line agent in invasive aspergillus disease
Minimal activity against mucorales or dimorphic fungi
Gram negative cocci
Neisseria sp
Moraxella
Gram positive bacilli/rods
Clostridium sp
Actinomyces sp
Coccobacilli
Gram positive coccobacilli - Listeria
Gram negative cocobacilli - Haemophilus, Legionella, Bordetella
Gram Variable/Pleomorphic - Acinetobacter
Macrolides
Azithromycin and erythromycin
Inhibit 50S subunit of ribosome
Clindamycin
Inhibits 50S Subunit ribosome
Linezolid
Inhibit protein synthesis
Inhibits 50S Subunit Ribosome
Aminoglycosides
Gentamycin, Amykacin, Tobramycin
Inhibit Protein synthesis
Inhibir 30S Subunit Ribsome
Bactericidal
Contraindicated in MG
Tetracyclines
Doxycycline
Inhibit protein synthesis, inhibiting 30S subunit ribosome
Quinolones
Ciprofloxacin, Moxifloxacin, Levofloxacin
Bactericidal
Highly bioavailability
Good tissue penetration (excluding CNS)
MOA: Inhibit DNA Gyrase/Topoisomerase
Trimethoprim Sulfamethoxazole
Inhibit folate synthesis and therefore nucleic acid synthesis.
Nitrofurantoin
Create free radicals, inhibit bacteria nucleic acid synthesis
Metronidazole
Create free radicals, inhibit bacterial nucleic acid synthesis
NO aerobic effect
Never use as mono-therapy apart from C diff
Disulfram effect
Bacterial Cell wall inhibitors
Beta-lactams
Glycopeptides: Vancomycin, Teicoplanin
Daptomycin
Polypeptides
Inhibit Nucleic acid synthesis
Inhibit DNA Gyrase or Topoisomerase - Quinolones
Inhibit folate synthesis - Trimethoprim (inhibits dihydrofolate reductase, same as MTX but specific for bacterial enzyme), Sulfamethoxazole inhibit folate synthesis.
Create free radials - Metro, Nitrofurantoin
Bacterial protein synthesis inhibitors
50S subunit inhibitors:
- Macrolides
- Clindamycin
- Linezolid
Inhibit 30S subunit:
- Aminoglycosides
- Tetracyclines
Beta-Lactams
Bacterio-CIDAL
Penicillins
Cephalosporins
Carbapenems
Monobactam - Aztreonam
Glycopeptide Antibiotics
Vancomycin, Teicoplanin
- Inhibit cell wall synthesis
Daptomycin
Depolarises cell membrane, bacteriocidal
Efffective against MRSA, VRE (faecalis and faecium)
Myopathy, neuropathy
Linezolid
MOA: Inhibits 50S subunit RNA pol, inhibiting protein synthesis
Effective against MRA and VRE
Only PO MRSA agent
A/E:
- Myelosupression, lactic acidosis, neuropathy, optic neuritis, serotonin syndrome.
4 highly resistant gram negative bacteria
Pseudomonas a
ESBL producing bacteria
Acinetobacter
Stenotrophomonas
Antibiotics with anaerobic cover
Metronidazole
Carbapenems
Beta-Lactam + Beta Lactamase
Clindamycin
Moxifloxacin
How to choose:
- Above diaphragm - Clindamycin preferred (metronidazole misses actinomyces and micro-aerophilic strep)
- Below Diaphragm - Metronidazole preferred
- to cover everywhere - Amox/Clav, Pip-taz, Carbapenem, Moxifloxacin.
Treatment of atypical infections
Macrolides - Azithromycin
Doxycycline
Quinolones
Gram positive cocci in clusters
Staphylococcus sp
Gram positive cocci in pairs and chains
streptococcus spp
enterococcus spp
Gram positive diplococci
strep pneumoniae
Gram negative coccobacilli
haemophilus influenzae
UTI with negative nitrite test?
Enterococcus
Staph saprophyticus
UTI with pH > 6.5
Suggests the organism produces a Urease:
- Proteus
- Klebsiella
- S saprophyticus
Troponemal Tests for Syphilis
Highly sensitive and specific, however once positive generally stays positive for life making interpretation difficult.
Think T
FTA
TPPA
TPHA
Syphilis specific Ab (CMIA/EIA)
Non-treponemal tests for Syphilis
Detects and QUANTIFIES Ab to non-specific antigens associated with ACTIVE syphilis infection.
Less sensitivity and specific than treponemal tests. But titre will decrease 4 fold with treatment, usually to 0.
However can also decline without treatment, making interpretation more difficult.
THINK NO T
RPR
VDRL
Treatment of Syphilis
IM Benzathine penicillin (1.8g / 2.4million U)
Duration:
- Primary, Secondary or Early Latent (<2 years) = 1 single dose, or 2 doses one week apart in 3rd trimester pregnancy.
- Late Latent = 3 x weekly doses
- Tertiary = 14 days of benzylpenicilin
If penicillin hypersensitivity - desensitisation is recommended, 28 days doxycycline if not possible.
Follow-up:
- Repeat RPR titre at 3, 6, and 12 months
- Successful treatment with 4 fold (or 2 titre) decline in Syphilis.
Algorithm for Syphilis Testing:
1 - Specific Treponemal Test - FTA, TPHA, EIA. If positive, you have been exposed to syphilis at some stage. proceed to non-treponemal test.
2 - Proceed to RPR or VDRL (non-treponemal test)
If Non-treponemal is negative, then a second alternative treponemal test is performed:
- If negative, then the initial test was likely false positive.
- If positive, than likely indicates infection and treat accordingly
If history of previous infection:
- Compare previous VDRL/RPR titres to determine if successful treatment or re-infection. (fourfold titre or 2 dilution change)
Staging of Syphilis:
Primary - Chancre
Secondary - systemic syndrome
Positive serology on test but no clinical symptoms/signs = Latent Syphilis
- Within 2 years - Early Latent Syphilis
- > 2 years - Late Latent Syphilis
(use previous serology, history of clear primary or secondary syphilis within 2 years, sexual debut)
Tertiary Syphilis:
- Gummatous disease
- Cardiovascular
- Neurological
Q Fever Facts
Caused by Coxiella burnetti
Gram negative obligate intracellular pathogen
Route of Transmission: Inhalation of droplets released by infected animals (sheep, cattle, goats, dogs, cats, birds, rodents, ticks - shed in birth products, urine, faeces, milk). Can also get by drinking raw milk.
Presentation:
- Non-specific febrile illness, constitutional symptoms.
- Incubation period 20 days
Diagnosis: Serology
Treatment:
- Doxycyclines
- Chronic: Doxycycline + Hydroxychloroquine
Exotic Infectins
Lyme DIsease - Borrelia burgforferi
Rickettsia autralis - Tick typhus
Brucellosis - Brucella
Most common form of TB resistance
Isoniazid Resistance is most common - present in 10% of australian isolates.
Standard short course therapy is not appropriate for these patients.
Standard Short Course TB Treatment
Intensive phase = 2 months of RIPE +/- pyridoxine (to prevent peripheral neuropathy)
Continuation phase = 2 months of RI
Only suitable if:
- bacteria are susceptible to RIP
- no meningitis or CNS disease, or complicated MSK disease.
- no extensive disease on CXR
Definition of Multi-Drug Resistant TB
Resistance to at least Isoniazid and Rifampicin (1-3% of Australian isolates)
Definition of Extensively drug resistant TB (XDR-TB)
MDR-TB + resistance to Quinolones and 2nd line parenteral drugs.
Usually treat with aminoglycoside amikacin
Treatment of TB Meningitis
Complicated
May need higher doses of Rifampicin to penetrate CNS.
May need addition of Moxifloxacin for CNS penetration
Use steroids for 6-8 weeks
Treat for extended duration 12 months.
Treatment of Extrapulmonary TB
Can have standard short course treatment except if:
TB Meningitis or CNS
Extensive MSK disease (Potts disease)
Miliary TB
HIV Infection
Ethambutol
Optic Neuritis
Monitor visual acuity and colour vision at baseline and then monthly.
More likely in those with renal impairment.
Rifampicin
Hepatitis
Orange Urine
Enzyme INDUCER - lowers efficacy of other drugs
Isoniazid
Rash
Liver enzyme elevation / Hepatitis
Peripheral Neuropathy - Pyridoxine B6 may prevent
Pyrazinamide
Hepatitis
Hyperuricaemia
GI upset
HIV and TB
Risk of IRIS
Treat TB first and then add HART
- 2 weeks if CD4<50
- 8-12 weeks if CD4>50
- At least 8 weeks regardless if TB CNS disease
Treatment of latent TB
Isoniazid monotherapy 9 months
Rifampicin monotherapy for 4 months
Rifampicin + Isoniazid for 3 months
Treatment of latent TB
Isoniazid monotherapy 9 months
Rifampicin monotherapy for 4 months
Rifampicin + Isoniazid for 3 months
Mechanism of Rifampicin
Inhibits bacterial RNA polymerase (same as rifabutin, rifaximin)
SImilar:
- Cytarabine - human RNA pol
- Aciclovir - viral RNA pol
Kaposi Sarcoma
Ulcerated lesions typically on lower extremity
Caused by Kaposi Sarcoma associated herpes virus (KSHV) also known as Human Herpes Virus 8
HHV8 also associated with primary effusion lymphoma and Castlemans DIsease (giant lymph node hyperplasia)
Merkel Cell carcinoma
Rare neuroendocrine tumour of the skin caused by POLYOMA VIRUS
Opportunistic Infections in HIV
CD$ 200-500:
- Herpes Zoster, Pneumococcla pneumonia, Oral Candidiasis, TB
CD4 < 200:
- PJP, Kaposi Sarcoma, NHL, PCNS Lymphoma
- Therefore give Bactrim <200
CD4 < 100
- - CNS Toxoplasmosis
CD4 <50
- Disseminated MAC - Therefore give Azithromycin 1gram weekly < 50
- CMV (retinitis)
- Crtyptocporidiosis
Strategies for ART in HIV
Start as soon as safe to do so.
Use 3 drugs from at least 2 different classes (usually 2 x NRTI + and INSTI, NNRTI, or boosted PI.
Data also supports the use of 2 drug regimen Dolutegravir + Lamivudine
Think about:
- Tenofovir - avoid in renal impairment and osteopenia
- Abacavir - test for HLAB5701
- In the presence of hep B co-infection treat with Tenofovir (Emtricitabine and Lamivudine also have some activity).
Initial Regimens for HIV
BIKTARVY = Bictegravir (BIC = INSTI), Tenofovir alafenamide (TAF = NRTI), emtricitabine (FTC = NRTI)
TRIUMEQ = Dolutegravir (DTG = INSTI), abacavir (ABC = NRTI), lamivudine (3TC = NRTI)
- Must be HLAB1507 negative and hepB negative
TRUVADA = Tenoforvir Disoproxil Fumarate (TDF) + Emtracitabine (FTC)
DESCOVY = TAF + Emtracitabine
DOVATO = Dolutegravir (DTG = INSTI), Lamivudine (3TC = NRTI)
- Not for individuals with HIV > 500 000c/ml, HBV co-infection, or before viral resistance testing has been done.
Protease Inhibitors in HIV
Darunavir
Atazanavir
Always are boosted with Ritonavir or Cobicistat
Major A/E is Increased CVD Risk
INSTIs in HIV
Raltegravir
Dolutegravir
Bictegravir
Cabotegravir - long acting injectable
Major A/E is Weight Gain
HIV PrEP
Tenofovir disoproxil fumerate (TDF) + Emtracitabine (FTC)
Can be On demand - prior to sex, and then 2 time daily. Good for infrequent exposures.
Can be daily.
3 monthly HIV tests and STI checks
Post Exposure prophylaxis (PEP)
Non-occupational exposure with KNOWN HIV status.
- Only recommended if source is not on treatment or has unknown viral load.
- If undetectable viral load known, then not recommended.
- Not recommended for any oral sexual exposure (low risk)
Non-occupational exposure to a source with UNKNOWN HIV Status:
- Not recommended for vaginal or oral intercourse. Not recommended for a non-intact skin or random needle stick injury.
- 2 drug regimen recommended for anal intercourse or needle sharing with MSM or from high prevalence country only.
Prophylaxis in HIV
Primary - <200 Bactrim, < 50 Azithro
Secondary - continue prophylaxis after induction treatment for OI until immune restoration on ART.
Cessation of prophylaxis:
- PCP, Toxo, Crypto - CD4>200 for 3-6m
- MAC - CD4>100 for 3-6m
- CMV - CD4 >100-150 for 6m
Japanese Encephalitis Epi
RNA Virus
Flaviviriadae family - along with Murrary Valley Encepnalitis, West Nile Virus
Viral life cycle involves CULEX mosquito transmitting virus between PIGS and WADING BIRDS. Humans are infected as end hosts.
Japanese Encephalitis CLinical
Transmitted by CULEX Mosquito
Risk if working with pigs or live within 4km of piggery
1% of cases develop encephalitis - parkinsonian features, asyymetrical limb paralysis, SIADH. 20-30% fatality rate if develop encephalitis.
Diagnosis - PCR, igM, MRI (Deep lesions)
Supportive care
Vaccinate:
- IMOJEV - live attenuated
- JESPECT / IXARIO - inactivated
