Infectious diseases Flashcards
Mode of transmission of each hepatitis vaccine
A = Food and drink contaminated with faeces of an infected individual. B = blood transmission. C = blood transmission. D = blood or sexual contact. E = raw/undercooked meat.
Which hepatitis’ are there vaccines for?
A, B (some protection over D)
Non hepatitis virus causes of hepatitis
Autoimmune
Alcohol
EMV and CMV
Short term/acute symptoms of hepatitis
Nausea Right upper quadrant abdo pain Fatigue + malaise Jaundice Myalgia and arthralgia
Which hepatitis virus’ cause acute and which cause chronic hepatitis and what time scale defines which it is?
Acute = All can occur as acute symptoms. Chronic = B, C, D.
Chronic = infection longer than 6 months.
Complications of chronic hepatitis
Cirrhosis
Liver failure
Hepatocellular carcinoma
Investigation for immunity to hepatitis B
HBsAb - Hepatitis B surface antibody (either from vaccine or previous infection). Vaccine injects HBsAg which mounts immune response and produces HBsAb to give immunity (as no HBeAg or HBcAg injected no chance of acquiring chronic viral hepatitis).
Investigation to show current Hep B infection
Abnormal LFTs Positive: HBsAg HBeAg (from replication) Viral load high on PCR HBcAb with esp high IgM
Treatment of acute hepatitis B
Self-limiting so no treatment.
Ways to spread Hep B
Risky sexual behaviours (HBV > HCV for sexual transmission)
Vertical - mother to newborn.
Sharing needles.
Blood transfusions and dialysis.
Treatment for hepatitis B
Nucleoside reverse transcriptase inhibitors.
Tenofovir or Entecavir.
Prevent DNA replication (can still produce cell proteins). Reduces HBeAg. Potentiates seroconversion and limits liver damage.
Ways to spread Hep C
Needle sharing
Needle injuries at work
Tattooing needles
Bloodstained toothbrushes
Symptoms of acute hep C
None, flu-like not worth seeing doctor about.
Extra-hepatic manifestations of hepatitis C
Glomerulonephritis Cryoglobinaemia Autoimmune thyroid disease Porphyria cutanea tarda Lichen planus
Ix for Hep C
Enzyme immunoassay and immnoblot assay for Hep C antibodies.
PCR for HCV RNA.
How many genotypes fo Hep C are there?
6🤙
Chronic liver disease with Hep C
1 in 3 with chronic HCV infection will get end stage liver disease.
Need close follow up for cirrhosis and HCC.
Tumour marker for hepatocellular carcinoma
AFP - alpha fetoprotein.
Treatment for Hep C
Is curative! Novel = Direct acting antiviral drugs. NS3/4A protease inhibitors e.g. Grazoprevir. NS5A inhibitors e.g. Velpatasvir. NS5B inhibitors e.g. Sofosbuvir.
Who are most at risk for chronic Hep B infection
Perinatal or early childhood infected patients.
Investigations for suspected viral hepatitis
LFTs - elevated ALT/AST, alk phos and bilirubin, low albumin. FBC - microcytic anaemia Coagulation - can have high INR/PT Serology Ultrasound of liver AFP for HCC Liver biopsy
Hep B = Serum HbSAg, HbS IgM antibodies
Investigations to show chronic Hep B infection
Positive: HBsAg HBeAb HBcAb esp high IgE Viral load lower on PCR
No HbsAb as they obviously cant clear the virus and HBsAb is the only antibody to resolve virus.
‘Resolved’ Hep B infection pathophysiology and investigations
4% a year resolve. This can occur after a chronic infection of many years or after an acute infection.
The only resolves when complete seroconversion from HBsAg to HBsAb.
Ix: positive for
HBcAb esp high in IgE
HBeAb
HBsAb
Difference between Hep B and Hep C
Hep B is a DNA virus and is harder to treat - never cured only resolved.
Hep C is a RNA virus so able to cure patients.
Investigations for Hep A
IgM antibody for HAV in acute illness and long term high IgG HAV antibodies.
Abnormal LFTs
Elevated serum bilirubin
Management of Hep A
Supportive care - fluids, good nutrition.
Hep A vaccine
IV immunoglobulins
Pathophysiology of Hep D
Can replicate independently once inside cell but require HBV surface antigen for propagation.
Organism for TB
Mycobacterium tuberculosis
Risk factors for TB
HIV Older age (weaker immune system) Vit D deficiency DM Immunosppression e.g chemo/steroids Silicosis and lung fibrosis disease Alcohol and smoking Poverty
S+S of pulmonary TB
Night sweats Haemoptysis Chronic cough Weight loss Fever Malaise, fatigue, anorexia
O/E: Tachypnoea High temp Hypoxia Clubbing Apical lung sounds
Investigations for pulmonary TB
3 x Acid Fast Bacilli of sputum sample.
If +ve = infective, if -ve doesn’t rule out TB, just less infective/bacteria present.
Blood PCR
CXR - fibronodular opacities in upper lobes with or without cavitation, Gonn focus from calcification and fibrosis around granuloma.
FBC - anaemia, raised WCC
Treatment for pulmonary TB
NOTIFY PHE!!!!!!!! Contact tracing.
Drugs: Isoniazid (H) Rifampicin (R) Ethambutol (E) Pyrazinamide (Z)
Isoniazid + Rifampicin for 6 months daily.
Ethambutol + Pyrazinamide for first 2 months daily only.
Test of cure CXR.
How to treat a TB patient who you are worried wont comply?
Directly Observed Therapy - higher drug doses are given 3 times a week. The patient is observed taking them.
Multi-drug resistant TB
Resistance to at least Isoniazid and Rifampicin.
Patients treated with range of 5-8 drugs for up to 2 years.
Side effects of HREZ drugs
Isoniazid - peripheral neuropathy, agranulocytosis.
Rifampicin - thrombocytopenia, orange urine, many drug interactions including warfarin, oral contraceptives, methadone!
Ethambutol - ocular toxicity.
Pyrazinamide - hepatotoxic, arthralgia, gout/hyperuricaemia.
Latent TB test
Tuberculin skin test / Mantoux test:
- Doesn’t discriminate against those who are vaccinated and those who have previous infection.
- Can get false negative if patient is immunocompromised.
ALTERNATIVE
Interferon Gamma Release Assay (IGRA):
- 2 types = QUANTIferon and T-Spot.
- Distinguishes between vaccinated and latent TB but will also be +ve with active/acute infection.
- Therefore need thorough clinical assessment and CXR.
Locations for extra-pulmonary TB
CNS - TB meningitis TB osteomyelitis TB lymphadenitis Abdominal TB Pericardial TB
Pott’s disease
TB osteomyelitis in the vertebrae.
Pathophyisology of HIV
RNA virus
Enters cells which express CD4 receptor. Mostly T-lymphocytes, macrophages and dendritic cells.
Inside the host’s cell the virus replicates using viral enzymes reverse transciptase and protease) and harnessing host’s proteins to form new viral particles.
Host’s immune system tries to destroy these viral infected cells leading to reduction in CD4 cell count.
Can have host’s immune system control the viral infected cells creating asymptomatic phase (+10yrs) where viral load stays at set point and steady gradual decrease in CD4.
When CD4 T-lymphocyte count is so low that the host is predisposed to opportunistic infections = acquired immunodeficiency syndrome (AIDS).
Risk factors for HIV infection
IVDU needle sharing Unprotected sexual intercourse Vertical transmission to baby Occupational needle stick injury Blood product transfusion e.g haemophiliacs before screening was introduced.
Differential diagnosis for acute primary HIV illness
infectious monoculeosis
S+S in acute, primary HIV illness
Fever Night sweats Myalgia + arthralgia Anorexia Nausea and diarrhoea Lymphadenopathy Maculo-papular rash on trunk and torso Weight loss
Things in a history to suspect HIV
Recurrent UTI Recurrent oral candidias Severe bacteria infections for unexplained reasons e.g. pneumonias. Herpes zoster history Persistent lymphadenopathy Social risk factors
Investigations for HIV/newly diagnosed HIV patient
HIV status via ELISA (p24 antigen), PCR HIV viral load CD4+ count - usually <450cells/mL Offer full STI screen Viral hepatitis antibodies/Blood born virus screen FBC - low Hb U+E LFT and synthetic liver function test esp before starting drugs. Bone profile Tuberculin skin test Urinanalysis
Window period for HIV status testing after exposure
4 weeks. Can get false negative if test immediately after exposure. Give post exposure prophylaxis.
Framework for HIV Management
HAART.
Drug classes used:
Nucleoside reverse transcriptase inhibitors.
Non-nucleoside reverse transcriptase inhibitors, Protease inhibitors.
Entry inhibitors
Fusion inhibitors
Most combinations use 2NRTI and 1PI or NNRTI.
99% reduction in viraemia in 8 weeks.
Can interrupt treatment and can manipulate Rx.
Monitor response with CD4+ count.
Non drug parts = annual flu vaccine, counselling and psych support, annual cervical screening for females, safe sex advice.
Pharmacology, side effects and examples of NRTI
Prevent DNA replication from virus’ RNA.
SE = hypersensitivity (fever/rash)
Examples = Abacavir, Zidovudine
Pharmacology, side effects and examples of NNRT
Prevent DNA synthesis but not as a analogue to nucleotide.
SE = nightmares, hepatotoxic.
Examples = Etravirine, Efavirenz.
Pharmacology, side effects and examples of protease inhibitors
Prevent production of functional proteins from polyprotein.
SE = hyperlipidaemia, diarrhoea, peripheral neuropathy.
Examples = Atazanavir, Darunavir
AIDS
Acquired Immune Deficiency Syndrome CD4+ count of <200cells/mL AIDS defining illness: Pneumocytis jirovecii pneumonia CMV retinitis TB Kaposi's sarcoma Non-Hodgkin's Lymphoma ect etc (many more)
HIV and pregnancy:
Pre-conception advice
Drug given to new born
Post-partum advice
3 months of undetectable viral load = untrabnsmittable to baby so can have NVD. If viral load is detectable have C/S.
Zidovudine for 4 weeks
No breastfeeding.
Prevention measure in HIV
Post exposure prophylaxis (Truvada)
Trials ongoing for pre-exposure prophylaxis.
NICE guideline for genotype 1 HCV
12 weeks. Sofosbuvir (NS5Bi) and NS5Ai Velapatasvir. get clearance of virus.
Virus associated with Kaposi’s sarcoma
Herpes simplex virus 8
Life cycle of malaria parasite
Host is infected when bitten by an infected female Anopheles mosquitoes.
Malaria sporozoite enters human via mosquito’s saliva.
The sporozoite travels to the host’s liver where it enters hepatocytes and matures to form schizonts.
Rupture releases thousands of meozoites into the blood of the host.
In the blood the meozoites enter RBCs and cause the clinical picture seen in malaria. They also mature in male and female gametes in the RBCs.
When a mosquito bites the host again they ingest the gametes in the blood and go on to create more sporozoites and spread the disease.
Species of malaria
Plasmodium falciparum - most prevalent and responsible for most deaths. Plasmodium vivax Plasmodium ovale Plasmodium malariae Plasmodum knowlesi (monkeys)
Complications of malaria
Cerebral malaria - seizures, coma. ARDS Jaundice Severe anaemia Hypoglycaemia AKI Splenic rupture
S+S of malaria infection
Presentation can be delayed. Fever Sweats +/- chills Headache Malaise, fatigue, anorexia Nausea, abdo pain, d+v Myalgia, arthralgia Sore throat Cough
WHO criteria for severe malaria
Impaired level of consciousness Resp distress Convulsions Circulatory collapse/hypovolaemic shock Pulmonary oedema Abnormal bleeding/DIC Jaundice Haemoglobinuria (red dark urine) Severe anaemia Hypoglycaemia Acidosis Renal impairment Hyperlactataemia Hyperparasitaemia (>2%)
Investigations of malaria
Giemsa-stained thick and think blood film microscopy. Thick to see if parasite present, and thin to look at morphology and species identification. Rapid diagnostic tests e.g. Antigen detection test FBC - low Hb Clotting profile - prolonged PT. U+Es LFT - elevated bilirubin BM Urinanalysis ABG
Management of malaria
NOTIFY PHE!
Based on WHO guidance.
Treatment of uncomplicated P.falciparum:
3 days of
Artemisinin-based chemo (ACT) e.g Artemether + Lumefantrine
Treatment of severe malaria:
IV Artesunate then 3 days or oral artesunate.
Beware of P.falciparum resistance (Chloroquine esp)
Differential diagnosis for malaria
Influenza flu Dengue fever Zika virus Chikungunya virus Enteric fever - thyphoid, parathyphoid, Salmonella infection.
Malaria prophyalxis
DEET spray (min 20%)
Mosquito nets
Covering clothes
Chemoprophyalxis e.g Doxycyline or atovaquone/proguanil (malarone)
Bacteria involved in meningococcal meningitis and meningococcal septicaemia
Neisseria meningitidis
Signs pointing to meningococcal disease rather than other meningitis
Skin rash - non-blanching purpuric, starts distal and moves proximal.
CV instability - hypotensive, prolonged CRT,
Bacteria in pneumococcal disease
Streptococcus pneumoniae meningitis.
Treatment of suscpected meningococcal disease
In community - IM benxylpenicillin.
In hospital - IV Ceftriaxone or IV Chloramphenicol if penicillin anaphylaxis Hx + Dexamethasone (esp if ?streptococcal cause)
Prophylaxis for close contact in meningococcal disease
If over 5yrs - Ciprofloxacin
If under 5 - Rifampicin
Treatment for Legionella pneumonia
IV Clarithromycin
Bacteria causing blood in stool
Any colitis can but sterotypically: Campylobacter jejuni E.coli Shigella Salmonella Yersinia
Antibiotics for C.difficile infection
Metronidazole
Vancomycin
Antibiotics for gastroenteritis
Not routinely prescribed - supportive care.
If any given commonly Azithromycin
How many blood cultures needed for infective endocarditis
3
Common bacteria in cellulitis and antibiotics used
Streptococcus pyogenes
Staphylococcus aureus
First line = Flucloxacillin
Treatment of Pneumocytis jiroveci pneumonia
IV co-trimoxazole
Prednisolone
A complication of starting anti-retroviral treatment when a patient is suffering from opportunistic infection
Immune reconstitution inflammatory syndrome (IRIS). Will cause massive inflammation at area of oppertunistic infection.
Where will IVDU patients get infective endocarditis
In the right side of heart e.g. tricuspid valve.
Empirical treatment for infective endocarditis
IV amoxicillin + gentamycin
If known S.aureas = flucloxacillin
Differentials for photophobia
Meningitis
SAH
Migraine
Pyrexia of unknown location
At least 3 weeks of fever with all investigations finding nil of note.
Differentials for night sweats
TB
Cancer (lung)
Infection (pneumonia, endocarditis)
Menopause
Fevers spiking every 24 hrs indicative of…
Malaria
Investigations to do before starting a patient on TB drugs
Eye test (ethambutol = ototoxic) LFT Renal function
Treatment for latent TB (picked up on IGRA)
6 months of Isoniazid or
3 months of Isoniazid + Rifampicin.
Doesn’t cure TB but reduces reactivation by 2/3.
Stain for Cryptococcus
India ink
Kaposi’s sarcoma
Malignancy of endothelial cells (vascular)
HSV8
Is an STI.
Granuloma
Aggreggation of epitheloid histiocytes.
Natural history of TB
TB infection enters lung and macrophages try and combat it but bacilli proliferate inside macrophage and forms granuloma. This can lead to dormancy until reactivation by triggers such as low CD4 HIV
Recent travel to conference, dry cough and deranged LFT. Ix and Mx
Legionella. Colonised in water tanks so comes out in air conditionings.
Urine antigen test, FBC, CXR (nothing exciting), sputum sample (gram negative rod).
Rx = IV Clarithromycin
Transmission of Leishmaniasis
Vector - female phlebotomine sandfly
Types of Leishmaniasis and clinical features
Cutaneous, mucocutaneous or visceral
Skin/cutaneous = most common, papules, skin nodules, ulcerations.
Mucocutaneous = oral and nasal mucosa ulcerations.
Visceral = affects spleen, liver and bone marrow = fever, weight loss, splenomegaly, pancytopenia, hypergammaglobulinaemia.
Ix and Mx for Leishmaniasis
Ix = FBC, LTF, creatinine, microscopy of tissue samples. Mx = Stibogluconate, amphotericin B, miltefosine.
Pathogen for Syphilis
Treponema pallidum
Spirochete, gram negative parasite.
Needs human body host to survive.
Transmission of Syphilis
Acquired - sexual, contact of a chancre, needles.
Congenital - from mother to fetus/new baby
Stages of acquired Syphilis
Primary = early stage, localised disease. Painless ulcers - CHANCRE at area where disease was acquired (genitals, hand). Resolve in 3-8weeks.
Secondary = dissemination of T.pallidum via lymph. Occurs 4-10 weeks after initial chancre. Lymphadenopathy, macular-papular rash on trunk and spreads to extremities, moist warm areas get CONDYLOMATA LATA at anus and perineum, hepatosplenomegaly. Meningitis, uveitis, glomerulonephritis. Systemic symptoms of fever, myalgia, malaise, headaches. Resolve 3-12 weeks.
Latent = asymptomatic disease but serology shows infection. Develop granulomas - GUMMA.
Tertiary = chronic end-organ damage 20-40 years after initial infection, occurs in 1/3 of untreated patients. Cardiovascular neuro and gummatous.
S+S of tertiary syphilis
Neurosyphilis = dementia, personality change, psychosis. Damage to dorsal column areflexia, paraesthesia, ataxia. Cardiovasc = aortitis, aortic regurgitation, aortic aneurysm, angina. Gummata = granulomatous lesions. Plaques, fibrous nodules mostly on bones and skin.
Ix for syphilis
HIV test!!!!
Cardiolipin serology via RPR or VDRL, correlate to disease activity. Positive within week of chancre appearance, but not specific. Can use to monitor effect of Rx.
Treponemal specific serology via EIA or TPHA assays, are positive for life but not correlated to disease activity.
Biospy/swab of infected lesion or lymph node for - Dark ground microscopy and PCR
FBC, LFT, U+E, LP and CSF serology, x-ray of bones.
Congenital syphilis
Most are asymptomatic at birth, develop symptoms in 5 weeks.
S+S = rash, lymphadenopathy, hepatosplenomegaly, condylomata lata, glomerulonephritis lots and lots.
Mx of syphilis
Benzathine penicillin. Single dose in primary, 3 doses (once a week) for latent. Can be used in pregnancy.
If penicillin allergic = doxycycline.
Neurosyphilis = Procaine penicillin + benzylpenicillin.
Pathogen in typhoid and parathyoid
Salmonella enterica (gram negative). Typhoid = serotype S typhi. Only reservoir is humans.
Presentation of typhoid
Week 1: FEVER, dry cough, relative bradycardia, (Faget’s sign), headache, malaise.
Week 2: Apathy, confused, swinging fevers (worse in evening, better in morning), rose spots on chest and abdo, green pea soup diarrhoea, furred tongue.
Week 3: Weight loss, pyrexia, confused, abdo distention, foul diarrhoea, weak. Complications of disease present.
Week 4: Could be slowly improving.
Ix for typhoid
Stool mc+s Blood cultures Widal test = serology for agglutinating antibodies against H and O S.typhi antigens. Not very good. FBC = normal WBC LFT = raised ALT and AST.
Mx for typhoid
NOTIFY PHE!!!!
Rehydration
Good hygiene
ABx azithromycin, ceftriazone.
Dengue fever cause, presentation, Ix and Rx.
- Spread by mosquitos.
- CFx = fever, skin flushing, arthralgia, headache, petechiae and purpura from haemorrhage fever variant.
- Ix:
FBC = low platelets, high WCC.
LFT = elevated AST and ALT.
Serum albumin = low (hypoalbuminaemia)
Serology = ELISA fro IgM and IgG - Rx = NOTIFY PHE, fluids, supportive care, monitor LFT, FBC, UOP, coagulation.
What is dysentery
Diarrhoea with blood +/- mucus.
Bacterial = Shigella.
4 ways to catch urine and what is each for?
- First catch in morning = TB PCR
- First catch of stream = STI
- Mid-stream = UTI
- Terminal = schistosomiasis
Viral Haemorrhagic fever
- Suspect with travel Hx. Incubation of 2-21 days.
- Increased exposure to bats (caves) and rodents.
- RNA virus’s e.g. Filoviruses.
- Diseases such as Lassa Fever, West Nile virus, Ebola, Argentine haemorrhage fever.
- S+S = FEVER, petechiae, conjunctival injection (red eye), myalgia, sore throat, headache, fatigue, N+V, hypotension, oedema, altered mental state.
- ISOLATE THEM IF YOU SUSPECT IT!
- Ix for malaria (GIEMSA thick and thin blood film) and blood RT-PCR (RNA virus) to ∆.
- Mx: prevent spread (barrier nurse, contact trace, notify PHE). Supportive with fluids, anti-emetic, analgesia.
What to do with positive HIV test within 4week window period
Confirm it with repeat test!
CFx of Kaposi’s sarcoma and what virus causes it?
Purple brown rash on shins
HSV8
Causes of headache in HIV +ve and how to Ix
Cryptococcal meningitis - India ink stain of CSF.
TB meningitis - AFB of CSF
Neurotoxoplasmosis - CT head
Also common Strep pneumoniae meningitis, tension headache, cluster headache!
Prophylactic treatment in HIV
When CD4 count <200
Cotrimoxazole for PCP, toxoplasmosis and bacterial infections.
Azithromycin for MAI lung disease
Gancylovir for CMV.
Blood borne virus risk of infection from needle stick injury
HIV = 0.3% HCV = 3% HBC = 30%
Mx of chlamydia and gonorrhoea
C = Azithromycin R = Azithromycin + ceftriaxone Im STAT dose.
Rash on soles and palms?
Secondary syphilis
What are warts associated with secondary syphilis and name some other skin presentations of syphilis
- Condylomata lata.
- Chancre scares
- Snail track ulcers in mucosa
- Rash on palms and soles.
Testing for syphilis
- Treponemal specific serology e.g. EIA or TPHA assays, are positive for life but not correlated to disease activity.
If negative no syphilis, if positive then do: - Non-treponemal specific e.g. RPR or VDRL, correlate to disease activity. Positive within week of chancre appearance, but not specific. Can use to monitor effect of Rx.
How does malaria cause the features of severe malaria e.g pulmonary oedema
Infected RBC aggregate and block blood vessels. This damages vessel walls. Allows leakage form vessels. Hence pulmonary oedema, cerebral oedema, DIC
Mx of Leishmaniasis
Stibogluconate
Complications of hookworm
Anaemia, malabsorption.
Mx of liver abscess (amoeba)
Metronidazole and drainage (anchovy paste pus)
Blood test in Schistosomiasis and Mx
Eosinophilia on FBC
Praziquantel
Name 4 non-malaria mosquitoes transmitted diseases
Dengue
Yellow fever
West Nile Fever
Chikungunya
Ix in suspected viral hemorrhagic fever
Malaria thick and thin GIEMSA blood film
FBC, U+E, LFT, clotting, blood cultures, BM
Isolate and get senior help!!
Prevention of Isoniazid induced peripheral neuropathy
Pyridoxine
