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120 Cards in this Set
- Front
- Back
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Reservoirs for Hep A? |
None. Bivalves concentrate. |
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What should be done with contacts of Hepatitis A? |
Case by case basis --> Immunise at risk contacts/relatives. |
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What is the problem with large reduction in HAV? |
Epidemic HAV outbreaks occur as cohorts who aren't immune. |
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Hep A Virology. DNA or RNA? How spread? Immunity? Incubation? |
Picornavirus. RNA.
Spread faeco-orally. Solid immunity after one attack. Approx 4 weeks incubation. |
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Most at risk of symptoms from HAV? |
Older people (>50) and those with pre-existing liver disease. |
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Prevention of HAV? |
Public Health infrastructure including point source Ix. Water and sewerage. Food. Active immunisation of IVDUs, prisoners, travellers etc. |
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HEV. Reservoirs? |
Huge variety of mammals and birds that possibly act as reservoirs. |
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How does HEV transmit? And with each G ... where do you get it? |
G1-G2 --> Faeco-Oral with drinking water. (G1 mostly in Tropical countries G3-G4 --> Zoonotic. (G3 in high income countries from raw sausages etc. |
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HEV. Clinical. Fatality? Who are more at risk of worse outcomes? Any chronic sequelae? Weird presentations? |
Longer incubation than HAV --> 5 weeks. Case fatality is around 1-3% but much, much worse for pregnant women (up to a quarter). Also fatality increases with age. Weird presentations like GBS can occur. |
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HEV in immunosuppression? Diagnosis? Outcomes? Tx? |
Dx --> Cannot trust serology. Need PCR. Outcome --> Can get chronic infection in 60% of patients and 10% will develop cirrhosis. Tx --> Interferon-Alpha and ribavirin are used. |
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HBV. How many infected. How many deaths per year. |
400 million infected. 2 million deaths |
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Natural Hx of HBV. Incubation period? What percentage of adults will clear the virus? Of those chronically infected? |
Huge range of incubation from 9 to 26 weeks More than 95% will clear the virus. 30% cirrhosis5-10% HCC |
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Pattern of age and HBV infection? |
Infants will tend to have no symptoms if infected with HBV but have a very high likelyhood of chronic infection. |
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HBV serology: Past infection Current infection Past immunisation Role of HBeAg? |
Past infection - anti HBs and anti HBc Current infection -HBsAg + anti HBc Past immunisation - ONLY anti HBs Although can be mutations and low HBeAg production but high HBV DNA. |
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Pattern of ALT and HBV DNA (Or surrogate HBeAg) in: Immune Tolerance. Immune Clearance Inactive Carrier Reactivation |
immune Tolerance - High HBV DNA and normal ALT Immune Clearance - High HBV DNA/HBeAg and high ALT. Carrier state - Low HBV DNA and normal ALT, production of anti HBe. Reactivation - High HBV DNA and ALT. Now converted to high anti-HBe. |
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Hep D. How is it spread? Superinfection - Outcome? |
Uses Hep B's sAg. Spread sexually or parenterally. Superinfection has high acute mortality |
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What are the two types of therapy for HBV? Examples of each, class and problems? How long are they needed for? |
Immunological --> Pegylated interferon alpha (1 year, approx £6k). Limited tolerance. Antivirals --> Nucleoside/tides (several years) Lamivudine (3TC) , NRTI --> Good initial response but cumulative resistance. Tenofovir --> Low resistance, can be nephrotoxic. |
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Regimens for Hep B vaccination?
Are boosters needed if previously seroconverted? |
0,1,6 months, 0,1,2,12 months, 0, 7, 21 days, 12 months |
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Global strategy for HBV has headed where? |
Increased immunisation. 69% of 2008 birth cohort received 3 doses. Supported by GAVI |
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Hep C Virology. What kind of virus? How can it present? Risk factors? |
RNA Flavirus.
Numerous genotypes 1-6. Asymptomatic and acute disease. |
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Is HCV readily transmissible sexually? |
Occurs but efficiency is low --> rare between long-term steady partners |
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HCV Natural History: Incubation Acute Illness? Cirrhosis? |
Average 6 weeks
Few have an acute illness (<20%) and usually mild. Most will become chronically infected (80%) Approx 10-20% will go on to have cirrhosis Much higher amount will have asymptomatic hepatitis (70%) |
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HCV diagnosis? Role of Anti HCV antibody? PCR? Imaging? What else do you want to know? |
HCV AB - Indicates past exposure HCV PCR indicates current viraemia. Can do fibroscan - Important for decisions Also want to know VL and genotyping for clinical decision making |
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How do we rationalise and ration Tx for HCV? |
Main issues are that we do not know how patient will progress and they can be asymptomatic. |
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Who do worse from HCV? |
Genotype 1, Men, Obese, Cirrhotics, Non whites |
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Advice for patients with HCV? |
STOP BOOZE Immunise/Test HAV/HBV Inform of potential for onward transmission |
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What are the 3 main hosts/reservoirs of cholera? |
Man, Shellfish, Plankton |
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Incubation period for Cholera? |
Hours to 5 days. |
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How long do you remain infectious with cholera? |
2-3 weeks.
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What is cholera seaonality linked with?
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Algal blooms --> often then associated with climatic events (e.g. El Nino) The algal blooms act as a catalyst for phytoplankton proliferation. |
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Cholera bacteriology. |
Classical and El Tor (each sub divided) -- Different asymptomatic carrier rates.
New V.Cholerae O139 in India. Likely to be next pandemiC. Also no immunity even if exposure to O1. Bacteria - Gram negative, comma shapped, aerobic. |
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Cholera pathogenesis.
How does the toxin work? |
2 subunits (A=Active, B=Binding) |
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Clinical spectrum of cholera? How many diarrhoea can be produced? Complications?
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Asymptomatic --> mild diarrhoea --> Severe dehydration/acidosis --> Renal failure ---> Death. Can loose up to 500-1000ml /hour ALWAYS CHECK GLUCOSE Mortality - 10% untreated (higher in Cholera sicca - little D/V, rapid collapse) |
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Diagnosis of cholera. (6) |
Usually clinical. "Darting vibrios" on dark-ground microscopy Movement inhibited by antisera (O1 for O1, O139 for O139) Culture is gold standard -- Difficult. Serotyping at referance lab RDTs are available (not great, use in outbreaks) |
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MGMT of Cholera |
Fluids --> ORS. IVI (Hartmaan's/RL)
ABx shorten Sx and reduce fluid loss. (e.g. Cipro/Cotrim |
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How do you decide between ORS and IVI for Cholera? |
Dehydration stage. For severe (lethargic ,floppy, dry mucous membranes) -- IVI, ABx |
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Cholera vaccine. Usefulness? |
Dukoral (killed plus recombinant cholera B subunit) OR Shanchol (no B subunit - does not require booster, cheaper)
Issues: Efficacy falls quickly in cholera endemic region, particularly in young children. However useful as herd effect in refugee camps. Target high risk groups (Pregnant women, young children and HIV) |
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ABx for Lepto?
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Mild Lepto -- Doxy. Can consider Amox. |
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Lepto. |
Pulmonary haemorrhage. Respiratory failure. |
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Weil Syndrome. |
Jaundice, renal dysfunction,hepatic necrosis, pulmonarydysfunction, and hemorrhagicdiathesis. (<5%) |
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Leptospirosis. Natural hosts? Humans? How long will animals shed organism in urine? Issue? |
Worldwide. Natural hosts are mammals (most, humans are incidental) Animals will shed in urine for weeks/months --> Environmental contamination. |
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Diagnosis of Leptospira? |
Difficult. Culture is very difficult (blood, urine, CSF) PCR --> Not totally sensitive Serology. |
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Bacteriology of Diptheria? Treatment? |
Gram positive bacilli. Benpen. |
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Diptheria. Incubation? What sort of spread? Presentation? |
Droplet. 2-5 days of incubation. Membranous pharyngitis with fever. Membrane is grey, thick and firmly adherent. Large cervical LNs with surrounding oedema. "bull neck" |
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Complications of diptheria? (3 topics) |
Cardiac - Heart block. Local mass effect --> Airways compromise/Stridor Neurological --> Peripheral neuropathy |
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Typhoid/Paratyphoid. Where can it be carried? How does it transmit? |
90% uncomplicted. 10% severe complicated. 10% + mortality with no treatment, <1% mortality if adequate treatment. |
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Basic S.Typhi bacteriology/pathophysiology. |
At peyer's patch --> Taken to mesenteric LN --> Spleen/Liver --> Shed via biliary system and reenters GI tract. |
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With Salmonella, where are the hotspots for Paratyphi A and NTS? |
NTS - SSA Paratyphi A - SE Asia |
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Most common group for imported enteric fever in the UK? |
Visiting friends and relatives and travelled abroad from UK (APprox 3/4 for both) |
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Sensitivity of PCR in Typhoid/Paratyphoid? |
Approx 97% |
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How does the Widal test work? |
Tests for agglutinating antibodies --> O (Lipopolysaccharide) H (Flagellar) Vi (Capsular Ag) Lots of false negatives and false positives |
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Use of rapid diagnostic tests in enteric fever? |
Lack sensitivity and specificity |
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Advantages of Ceftriaxone in Typhoid? |
Safe, efficacious, limited resistance, coverage of other organisms (Typhus), Once daily dosing. |
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Cefixime in Typhoid? Advantages and disadvantages? |
Disadvantges --> Slow to get better. Expensive. Twice daily. Limited evidence. |
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Azithromycin in Typhoid. Advantages and disadvantages? |
Advantages: Safe, oral, little resistance, concentrated in bile, Disadvantges: Expensive. Poor coverage of other pathogens, increasing resistance |
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Complications of severe enteric fever.
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Bowel perforation, Encephalopathy, GI bleeding. |
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Use of steroids in Typhoid? |
Dexamethasone in severe typhoid fever. |
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Control of typhoid fever? (5) |
Case control. Case findings. Treatment Treatment of carriers. Vaccines? |
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Treatment of chronic carriers of typhoid? |
Amox/Amp 3 months Cipro BD for 28 days Cholelithiasis - Cholecystectomy may be required. |
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Use of typhoid vaccines? Efficacy? |
To control epidemics
Public health measure for endemic disease Vi vaccine - Efficacy 60-70%, drops off. (IM) |
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How to classify salmonella? |
Typhoidal salmonella: Paratyphi A Typhiumrium Enteritidis |
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Spectrum of Salmonella disease and associations with clinical spectrum. |
Generalists such as Enteritiditis and Typhimurium are usually more enteric/diarrhoea disease with low mortality. |
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NTS spectrum: Most at risk of worse disease? |
Diarrhoea Focal infection -Bones and joints -Endovascular -Meningitis
Immunocompromised. |
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Antibiotics for salmonella gastroenteritis. Useful?
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12 trials. No evidenceof clinical benefit of ABx therapy in healthy children/adults with non severe salmonella. |
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SSA. NTS. Associations Mortality |
Fever in 95% of cases
Anaemia Pneumonia in 60% of children and 30% of adults - Co-infection. Diarrhoea Mortality - Really high! Up to 30%. More than |
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Tx of NTS. Issues? Usual therapies? |
ABx resistance common. Recurrence with the same strain. Tx - Fluroquinolones and cephalosporins. |
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NTS and HIV Issues with gut mucosa, cytokines and antibodies? |
CD4 depletion in gut mucosa. Impaired serum kliling of NTS in HIV. |
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Other risk factors for poor prognosis in NTS in african children apart from HIV. |
Malaria - Macrophage dysfunction Sickle cell Deficiency of anti-salmonella IgG Malnutrition Protection in first 3-4 months with trans placental antibodies. |
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Lassa Fever. Where? How transmitted? How presents? Issues? |
Very prevalent in Sierra Leone. Often presents with pharyngitis and retrosternal chest pain. |
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Tx of Intestinal Protozoa |
Crypto homonis/parvum - Difficult. Nitazoxinide or Azithro
Blastocystitis Hominins - Nitazoxinide Cyclospora and Cystoisospora - Cotrim. Balitinium Coli - Tetracycline. (Can be lifethreatning colitis) All watery diarhoea |
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Anthrax.
Microbiology Distribution Reservoirs? |
Gram positive spore former. Worldwide distribution Zoonosis of herbivores. Tough spores that are infective |
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How can Anthrax appear in a population? |
Imports of bonemeal that goes into Gardens and animal feeds. Imports of hides/wool etc. |
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What are the routes of anthrax infection in man. 2 forms of anthrax. Any insect involved? |
Spores --> GI (From infected meat or contaminated water), Pulmonary (spore-laden dust) or cutaneous (via lesion) Role of fly in spreading from terminally infected animal or carcass after death. |
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Risk factors with anthrax. |
Can have endemic anthrax. Occupational --> Working with animal hide etc. Outbreaks from animals. (e.g. case of reindeer recently) |
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Diagnosis of anthrax. (4) |
Isolate from many body fluids Culture on blood agar. Gram Positive rods PCR confirm |
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Pathophysiology of anthrax. (5) Not details of toxin (Different question) |
Ingestion of spores. Taken up by macrophages. Spores germinate and create vegetative bacilli. Bacilli release toxin (pX01) |
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Anthrax toxin.
How many components. What are they called. What do they do. |
3 components PA - Protective antigen LF - Lethal factor EF - Oedema Factor PA binds to cell receptor for entry LF+PA = Lethal toxin EF + PA = Oedema toxin Toxins cause cell death. |
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Clinical presentation of anthrax (4) |
Cutaneous (95%) GI (rare) Inhalational Meningeal |
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Cutaneous anthrax. Where do the spores inoculate? Where does it commonly affect? How does it present? Mortality? |
Spores inoculate subcutaneously. Affects hands, forearm and head commonly. Small painless papule with increasing ulcer with marginal vesicles. |
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Weirder and wonderful anthrax presentations: (4) |
Oropharyngeal: Adenopathy, ulceration etc. Intestinal: Fever, malaise, abdo pain --> Ascities, acute abdomen, shock Inhalational Antrhax: Wool sorters disease. Haemorrhagic adenopathy/mediastinitis. Commonly get meningitis. Meningitis: Poor outcome. |
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Anthrax treatment and prophylaxis: |
Cipro IV Oral: Cipro/Doxy/Penicillin PEP - Cipro or Doxy for 30 or 60 days |
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Family of rabies viruses? One virus that gives clinical disease? RNA or DNA? |
Rhabdoviridae. Rabies virus, Duvenhage, European bat Lyssavirus Type 1 and 2, Australian bat Lyssavirus
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Rabies pathogenesis? |
Bitten --> Incubation period 20-90 days Centripetal, retrograde transport of virus. |
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Earliest clinical features of Rabies? 2 sites |
Skin --> Itching, pain, parathesia in dermatome of inoculum (Common!) Systemic --> Fever, insomnia, anxiety, headache |
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Clinical features of FURIOUS rabies. All neurological (7) |
Encephalopathy Autonomic Stimulation --> Salivation, frothing, priapism Spasms Hydrophobia/Aerophobia. Cranial Nerve lesions III, VII, VIII Paralysis Coma |
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Clinical features of paralytic rabies? |
Ascending paralysis --> Loss of reflexes Fasciculation Sphincter dysfunction Fever, sweating. Bulbar/respiratory paralysis. Survive <30 days |
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Diagnosing rabies. 4 different sites and methods. |
Can use different samples: Skin biopsy --> Ag Saliva/Tears --> Virus isolation CSF/Serum - Serology CSF - PCR |
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Treatment of established rabies. |
Industrial doses of sedatives. |
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How can we evaluate risk in Rabies? |
1. Where is bite - Intact skin? 2. Nature of bite - during play or unprovoked. 3. Animal species - Vaccination Hx of animal. 4. Immunohistochemistry of dog brain. |
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First aid for animal bites? (4) |
Clean wound as soon as possible with soap and detergent for 10 minutes. Don't suture Give tetanus. |
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Efficaciousness of rabies vacine post exposure when asymptomatic? |
100% |
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Pre exposure vaccination for rabies. Why? When? What? |
TO simply post exposure vaccination if bitten. Give at day 0, 7 and 28. Can give IM or intradermal |
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Post exposure vaccination (rabies) if NO Pre exposure vaccination. |
Standard (5 vials, 5 visits) 0, 3, 7, 14, 28 Alternative (4 vials 3 visits) 2 vials on day 0 1 vial 7, 21 |
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Why do we give passive immunisation in post exposure in Rabies? Who do we give it to? What forms? Risks? |
Covers first 7 days whilst antibody against vaccine is raised. Both human and equine Ig available |
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Recommendation for post exposure if pre vaccinated in Rabies. |
IM/Deep subcut vaccination at day 0 and 3 (Changing to just 1 dose) |
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Shigella
Basic micro. How many organisms to cause disease? |
Gram negative, facultative anaerobic rod. 4 groups (A = Dysenteriae, B=Flexneri, C Boydii, D Sonnei) Only 10-100 organisms needed to cause disease. |
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Pathophysiology of Shigella. |
Infects M cell and works its way along the epithelium |
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Chronic diarrhoea. Definition. Causes? Small bowel diarrhoea. Most frequent aetiology? Most frequent mode? Large bowel --> Most frequent cause? |
Chronic >4 weeks. Protozoa, helminths. Small bowel. Often viral. Secretory (e.g. Cholera). Large bowel - Inflammatory (often neutrophils in stool). |
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Clinical pointers to Shigellosis. (5) |
0-2 days incubation Short course Fever is common Abdo pain is common Progression to dysentery in a subset of patients |
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WHO MGMT of Shigellosis. (5) |
ORT Admit to hospital if malnourished. ABx recommended by WHO. AVOID antimotility ZINC. 10mg for 10 days <6. 20mg for 10 days >6 months |
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ABx for Shigellosis. |
Quinilones for 3 days. |
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Tetanus. Basic epi |
Gram positive, spore forming, obligate anerobe. Epi--> Tropical/Developing countries. Neonatal half the cases with 34000 deaths in 2015. Vaccination has had a huge effect. |
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What are the two main toxins that tetanus produces? |
Tetanospasmin --> Binds to presynaptic membrane --Prevents synaptic vesicles binding and transmitter release. This then travels retrogradely (centropetal) along axon --> can enter blood and lymphatics. |
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What are the 4 main subtypes of clinical presentation of tetanus. |
Local Generalised Neonatal Cephalic |
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Incubation time of tetanus. |
Approx 8 days.
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Generalised tetanus. Clinical features. Complications? Mortality? |
Painful spasms - precipitated by external or internal stimuli. Trismus Risus Sardonicus Autonomic dysfunction - Haemodynamic instability, sweating, pyrexia, arrythmias Mortality can be up to 50%. Takes up to 4 weeks to fully recover! |
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Neonatal tetanus. |
Stump care --> sometimes not the cleanest cut. Occurs 3-24 days after inoculation. SEVERE neurological sequelae |
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Localised form of tetanus. How long can it last? |
Can be very mild with regidity of muscles near site. Can progress to generalised form. |
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Tx principles of tetanus: (6) |
Debride wound. Supportive care - especially cardio + resp SEDATE Quiet nursing care Antibiotics (Metro) Tetanus Ig (Human and Equine tetanus - Human better) |
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Prevention of neonatal tetanus: |
Give a single dose tetanus toxoid in pregnancy, ideally 3 doses in total during pregnancy. 5 courses in total. |
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RFs for pneumonia? (8) |
Cigarette smokers Immune deficiency Age Malnutrition Liver/RF/Diabetes Steroids Prior viral infection Inflammatory lung disease |
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Ways to reduce pneumonia. (5)
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Vaccination Nutrition --> zinc in Children Structured early diagnosis - IMCI in children Better case MGMT Environmental changes --> Tobacco, household smoke, hand washing |
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How to rule out asthma? Anything to help confirm in low resource settings? |
Absence of : Wheeze, resting dyspnoea and nocturanl dyspnoea. To confirm: Peak Flow variability --> PPV 85%, Spirometry with reversibility PPV 91% |
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Brucella Micro |
Gram negative coccobacillus
Intracellular Has LPS Complex immune responses |
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How is brucella transmitted? |
Inhalation Ingestion of dairy products Direct contact Other e.g. sexual |
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What clinical syndromes with brucella? |
Asymptomatic Acute Subacute Chronic >6 months Hypersensitivity |
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What Sx with Brucellosis? |
MSK - Monoarthritis, Myalgia, Difficulty walking Spinal disease (In old men) - Can be uncomplicated or complicated. |
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Signs in brucella? |
Osteoarticular Hepatosplenomegaly 1/4 Lymphadenopathy Orchitis 10% |
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Diagnosis of brucellosis |
Culture - Any fluid! Keep for 6 weeks as slow growing + Serology |
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Adult Tx of brucellosis?
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Uncomplicated acute disease--> 6 weeks. Chronic/Complicated 3 months 2 drugs from doxy/rif/cotrim/gent |
