Acute Infection Flashcards

Question

What Organisms can cause IE?

Answer 1

The overall causative agents in IE are well documented and have been relatively stable, based on population-based studies over time. The most common pathogens are listed below; these together with any underlying risk factors indicate the most likely causative organism:[2] ``` Viridans group streptococci Staphylococcus aureus Enterococci Coagulase-negative staphylococci Haemophilus parainfluenzae Actinobacillus Streptococcus bovis Fungi Coxiella burnetii Brucella species Culture-negative Haemophilus species, Actinobacillus actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens, and Kingella species (HACEK). Patients who develop native valve endocarditis in the absence of intravenous drug use commonly present with viridans group streptococci, enterococci, or staphylococci, with other pathogens being less frequent. Intravenous drug users often present with right-sided valvular involvement and are more likely to have S aureus, streptococci, gram-negative bacilli, or polymicrobial infections.[2] ``` Prosthetic valve endocarditis is most commonly caused by coagulase-negative staphylococci, S aureus, enterococci, or gram-negative bacilli. It should be noted that early prosthetic valve endocarditis is often caused by Staphylococcus epidermidis.[2]

Answer 2

Bacteria that enter the bloodstream exist in a free-floating planktonic state. Most osteomyelitis is caused by biofilm-forming bacteria. These bacteria express surface components called adhesins that bind to proteins found in host tissues. Once attached, the bacteria produce a polysaccharide extracellular matrix, forming a biofilm.Once sufficient numbers of organisms are present in the biofilm, a complex system of cell-to-cell signalling develops, known as quorum sensing. This controls further development of the mature biofilm. It may also propagate the spread of infection by controlling separation of fragments of this biofilm which seeds to local sites. Some of the organisms in biofilm are able to enter a dormant state with minimal cellular division. In this state, antibiotics that act on cell division are ineffective. Clinical presentation is highly variable Septic arthritis tends to present with the rapid onset of pain, swelling and redness in a single joint Prosthetic joint infection may present with joint pain & evidence of inflammation at the surgical site Vertebral osteomyelitis presents with back pain & may progress to cause neurological signs Chronic osteomyelitis often causes a sinus which does not heal

Answer 3

``` Bedside tests Fever is often absent Blood tests FBC, U&Es, CRP, blood cultures Microbiological tests Joint aspiration, bone biopsy, tissue biopsy, sonication of excised prosthetic material Radiology Plain X-rays, CT scans, MRI scans ```

Answer 4

**Presentation:** - Purulent monoarthritis and/or - Triad of tenosynovitis, dermatitis (papules, pustules, necrotic lesions) and asymmetric migratory polyarthralgia - May occur several days to weeks following initial infection **Risk factors:** - Female sex - HIV infection - Menses - Low socioeconomic or educational status - Pregnancy - Multiple sexual partners - SLE - Complement deficiency **Diagnosis:** - Blood cultures (may be negative) - Synovial fluid analysis (joint aspirate) - Gram stain will show inflammatory effusion with neutrophil predominance plus or minus gram negative diplococci - Culture & sensitivity testing - NAAT PCR (if available and validated for synovial fluids) **Treatment:** - Intravenous ceftriaxone 2 weeks with appropriate oral switch for further 4 weeks - Joint drainage for purulent arthritis (may need to be repeated several times) Of note going back to the original presentation - Parvovirus B19 infection tends to cause a symmetrical polyarthralgia - Disseminated gonococcal disease tends to cause an asymmetrical and migratory joint symptoms - This case highlights the importance of taking a full medical history including sexual history

Answer 5

Native-Stap aureus,strep,clostridium.Neisseria gonorrhea,E-coli Prosthetic early-Staph,strep,Enterococci Late Coagulase negative staphylococci

Answer 6

Acute-<3 months, acute pain, fever,red swollen joint,Stap,ecoli are the causes Antibiotics-Courses of antibiotics need to be relatively prolonged Four weeks for septic arthritis At least six weeks for vertebral osteomyelitis & prosthetic joint infections Prolonged courses of iv therapy may be delivered via “OPAT” clinics Oral therapy may be as effective as iv therapy in many cases Osteomyelitis-Flucloxacillin Management-DAIR(Debridement,antibiotics and implant retention) Chronic-months to years, present with chronic pain, loosening prosthetic, sinus tracts.Causes include coagulase negative staph Surgical management-Complete removal of prosthesis in stage 1 and 2

Answer 7

Sustained or recurrent pyrexias for ≥3 weeks No identified cause after evaluation: in hospital for 3 days ≥3 outpatient visits ‘Classic’ Nosocomial Immunodeficient HIV ``` Possible Classic causes- Infection Abscess Infective endocarditis Tuberculosis Complicated UTI ``` ``` Geography/travel Melioidosis-Asia,Australia RA SLE Possible Nosocomial causes-Catheters/devices Thrombophlebitis UTI/RTI Drug fevers C.Diff ICU – ventilators, ET tubes, NG tubes Stroke-remodelling of brain tissues ``` ``` Immunodeficiency-Cell-mediated immunodeficiency Congenital Biologic/immunomodulatory therapies Neutropaenia Haematological disorders Chemotherapy < 500 neutrophils/µl N.B. blunted ‘typical’ inflammatory responses-might not be able to generate purogens N.B. lack of radiological changes ```

Answer 8

``` Laboratory Blood cultures Blood-borne viruses (BBV) – HIV/HBV.HCV Blood films – cells, parasites Serology FBC – differential U+E/LFT/bone chemistry TFTs Inflammatory markers – CRP, ESR, ALP Auto-antibodies – ANA, dsDNA Stool, urine, sputum, swabs Ascitic/pleural/synovial fluid Bone marrow Biopsy Imaging CXR US – liver/spleen Cross-sectional CT HRCT CT PET Labelled white cell scan (scintigraphy) Bone scan MRI ```

Answer 9

Infectious factors: microbes and microbial products G- bacteria: Lipopolysaccharide (LPS)/Endotoxin G+ bacteria: Exotoxins; Peptidoglycans Viruses Other microorganisms Non-infectious factors: Antigen-antibody complexes Complement Non-infectious inflammation-genesis irritants Drugs – antibiotics, steroids, chemotherapy agents ``` Fever-inducing cytokines: TNF IL-1 IL-6 IFN Derived from: mononuclear cells macrophages T-lymphocytes Kupffer cells endothelial cells tumour cells ``` Sustained-Parenchymal and interstital infections -Pneumonia,UTI,Typhoid,Brucelosis Intermittent-Abcess on lung brain liver ,intermittent sepsis,empyema Remittent-Active IE,blood stream infections Relapsing-usually have intervals of 24 to 48 hours for example in malaria,parasitic infections

Answer 10

he causative organism is almost always clostridial and is typically Clostridium perfringens. It is important to note that having a peripheral vascular disease increases the risk of developing gangrene of all causes. C perfringens is a Gram-positive spore-forming bacillus.

Answer 11

Typhoid and paratyphoid are caused by Salmonella typhi and Salmonella paratyphi (types A, B & C) respectively. They are often termed enteric fevers, producing systemic symptoms such as headache, fever, arthralgia They are aerobic, Gram-negative rods which are not normally present as commensals in the gut. Features initially systemic upset as above relative bradycardia abdominal pain, distension constipation: although Salmonella is a recognised cause of diarrhoea, constipation is more common in typhoid rose spots: present on the trunk in 40% of patients, and are more common in paratyphoid Possible complications include osteomyelitis (especially in sickle cell disease where Salmonella is one of the most common pathogens) GI bleed/perforation meningitis cholecystitis chronic carriage (1%, more likely if adult females)

Answer 12

However, potential complications can include hydrops fetalis and fetal death. The risk of these complications is similar in symptomatic and asymptomatic women with parvovirus. mmediate serological testing for parvovirus B19 is required for all pregnant women in contact with someone with a rash consistent with parvovirus.

Answer 13

The classic triad of sore throat, pyrexia and lymphadenopathy is seen in around 98% of patients: sore throat lymphadenopathy: may be present in the anterior and posterior triangles of the neck, in contrast to tonsillitis which typically only results in the upper anterior cervical chain being enlarged pyrexia Other features include: malaise, anorexia, headache palatal petechiae splenomegaly - occurs in around 50% of patients and may rarely predispose to splenic rupture hepatitis, transient rise in ALT lymphocytosis: presence of 50% lymphocytes with at least 10% atypical lymphocytes haemolytic anaemia secondary to cold agglutins (IgM) a maculopapular, pruritic rash develops in around 99% of patients who take ampicillin/amoxicillin whilst they have infectious mononucleosis

Answer 14

Symptoms typically resolve after 2-4 weeks. Diagnosis heterophil antibody test (Monospot test) - NICE guidelines suggest FBC and Monospot in the 2nd week of the illness to confirm a diagnosis of glandular fever. Management is supportive and includes: rest during the early stages, drink plenty of fluid, avoid alcohol simple analgesia for any aches or pains consensus guidance in the UK is to avoid playing contact sports for 8 weeks after having glandular fever to reduce the risk of splenic rupture

Answer 15

mmunosuppression can cause a false negative result - including in sarcoidosis, steroid use, AIDS and lymphoma. False positive-BCG,Immunity to TB

Answer 16

post viral-Staph Aureus | Alcoholics-Klebsiella

Answer 17

Features the disease typically has a prolonged and gradual onset flu-like symptoms classically precede a dry cough bilateral consolidation on x-ray complications may occur as below Complications cold agglutins (IgM): may cause an haemolytic anaemia, thrombocytopenia erythema multiforme, erythema nodosum meningoencephalitis, Guillain-Barre syndrome and other immune-mediated neurological diseases bullous myringitis: painful vesicles on the tympanic membrane pericarditis/myocarditis gastrointestinal: hepatitis, pancreatitis renal: acute glomerulonephritis Investigations diagnosis is generally by Mycoplasma serology positive cold agglutination test Management doxycycline or a macrolide (e.g. erythromycin/clarithromycin)

Answer 18

- Infection: TB, abscess, endocarditis, osteomyelitis, HIV, any other infection. - Lymphoproliferative disease. - Drugs: antidepressants, antipsychotics. - Endocrine: thyrotoxicosis, diabetes. - Others: menopause, anxiety, idiopathic hyperhidrosis.

Answer 19

Dengue Chickengunya zIKA

Answer 20

Warning signs-abdominal pain and tenderness,Persistent vomiting and diarrhoea,clinical fluid accumulation,mucosal bleeding,tender hepatomegaly,lethargy,Increase HCT and reduced platelets Severe Dengue Plasma leakage Organ impairment-shockAST/ALT>1000,CNS,heart Severe bleeding

Answer 21

NSAIDS and ibuoprofen increases the risk of bleeding.Acetoaminopen(Panadol)and sponging can be used

Answer 22

Febrile-dehydration Critical -plasma leakage, saddle back fever Convalesce-risk of fluid over load Pathophysiology-Affects endothelial glycocalyx layer

Answer 23

Febrile phase=Crystalloid Critical phase=Crystolloid,(FFP,Albumin,packed red cell,DIVC regime if severe) Recovery-stop fluid infusion and allow fluid resorption

Answer 24

naat RT-PCR NS1 antigen ELISA-IgM,IgG serology < 5days from onset of fever-RT-PCR,NS1 antigen >5 days-IgM(recent infection,IgG (past infection) RT pcr +IgM or IgM + NS1 extend the window of detection to 10 days post fever

Answer 25

gall bladder wall thickening

Answer 26

Spotted fever group Typus Scrub typus Scrub typus An acute, febrile, infectious disease which is caused by the organism Orientia tsutsugamushi. Source of infection--------Rat Route of transmission-----Trombiculid mites Susceptible population----All susceptible Spread by haematogenus or lymphatic system Epidemic features----------Tsutsugamushi triangle Clinical features Eschar(inoculation), regional lymphadenopathy, fever, Maculopapular rash, leukopenia

Answer 27

Tsutsugamushi triangle North: northern Japan and far-eastern Russia South: to northern Australia West: to Pakistan and Afghanistan

Answer 28

Epidemiology data：Visit the endemic area during the past 3weeks. working, camping or sitting on grass Clinical manifestation：Eschar,regional lyphadenopathy, fever, maculopapular rash, leukopenia, failed therapy with common antibiotic drug. Laboratory examination：Weil-felix reaction with titers beyond 1:160 or fourfold rise during the course of disease. Eschar Probability: Higher than 60%. Location: Axillary fossa, inguinal region, perianal region, scrotum, buttocks and the thigh. Appearance: an ulcer surrounded by a red areola, is often covered by a dark scab. Maculopapular rashes Onset: Appear at the end of the 1st week, lasts 3~7d. Location: Chest, abdomen, whole trunk, or upper and lower limbs. rarely involves the face, palms and soles. . ``` Haematology: Leukopenia Normal of WBC, Elevation with some complications. Biochemical: Injury of liver function, CRP ``` Weil-felix: Can be positive as early as 4th day after onset. >1:160 or increase 4 times during the course. Easy for operation but poor for specialization. IFA (Indirect Fluorescent Antibody): Almost the gold standard. Positive at the end of the 1st week. Last for years. IIP (Indirect Immunoperoxidase Test): Comparable to those from IFA. More available. Culture: Mouse is usual experimental animal. Spleen and liver are stain with Giemsa. PCR: Detect the orientia DNA Not routinely available

Answer 29

Ddx-Epidemic typhus: occur in winter and spring, bite by louse, Weil-felix with OX19 is positive. Typhus: Slow onset, persistent high fever, confusion, bradycardia, digestive symptoms, rose rash, no eschar, widal test positive. Blood culture of typhus bacillus is positive. Leptospirosis: Tenderness of calf muscle, microscopic haematuria Treatment Sensitive antibiotics decrease fatality from as high as 30 % (untreated) to 2%. 　　　　　 General treatment Supportive IV Fluids Intensive nursing care and prevent complication Chloramphenicol : 2g per day for adult, or 25mg/kg of bw per day for children. Doxycycline: 0.2g per day for adult. (tetracycycline alternative) Azithromycin 500mg daily. Roxithromycin: 0.6g per day for adult, 2~3mg/kg/d for child Strains resistant to doxycycline and chloramphenicol Combination therapy with doxycycline and rifampicin should be used if resistance suspected Azithromycin Prevention Source of infection: Rat Routes of transmission: Trombiculid mite Protect succeptibility: Avoid being bitten No effective vaccine against scrub typhus Prophylactic antibiotics ? Only in special situations perhaps! Few evidence

Answer 30

``` C.difficile MRSA CAUTI MSSA bacteraemia Indwelling catheter (line) related infections HAP and VAP Surgical site infections GI infections eg. norovirus as part of an outbreak Candida auris CPE (carbapenemase producing enterobacteriaceae) Antimicrobial resistance- others ESBL GRE/VRE ``` ``` Other transmissible infections: MDR/XDR TB VHFs (eg. Lassa fever, Ebola) SARS/COVID-19/MERS vCJD BBVs (hepatitis B/C, HIV) ``` - Healthcare environments can be a reservoir for organisms which have the potential to cause health care associated infections (HCAIs) - HCAIs are associated with increased morbidity and mortality and are estimated to cost the NHS around £2.7 billion per year. (1) - Therefore imperative to have collaborative working between designers, architects, engineers, facilities managers and the infection and prevention control (IPC) teams to create a safer environment for patients and staff.

Answer 31

Health & Safety at Work Act 1974 COSHH (Law on the Control of Substances Hazardous to Health) Workplace Regulations Building Regulations HTM’s (health technical memoranda) & HBN’s (health building note) HTMs-Comprehensive advice and guidance on the design, installation and operation of specialised building and engineering technology used in the delivery of healthcare. HBNs-Building note detailing each stage of a project, from initial concept through to post-project evaluation, in relation to infection control. ``` IPC team including DIPC (Director of Infection and Prevention Control) Microbiologists Domestic team Estates team including engineers Architects ``` Members from each team meet to discuss, monitor and improve infection control in various areas, such as water and ventilation.

Answer 32

Important to have appropriate ventilation to prevent airborne infections Airborne transmission Spread of an infectious agent caused by the dissemination of droplet nuclei/aerosols (≤5μ) that remain infectious when suspended in air over long distances and time (vs contact or droplet transmission >5-10μ) Ventilation is a means of removing and replacing the air in a space Dilution of contaminants Clean airflow path Control of Hazards-removal of gases moisture,odors Comfort Clean air flow paths positive (neutropenic)and negative pressure rooms(infection) Ultra clean ventilation

Answer 33

Pseudomona's Team of specialists that creates, implements, and maintains a Water Safety Plan (WSP). WSP - designed to ensure that the water used in hospitals and similar healthcare settings is safe to use by patients, staff and visitors, and poses minimal risk of infection from waterborne pathogens

Answer 34

Meticillin Resistant Staphylococcus aureus Staph aureus is a Gram positive bacterium that causes infections such as cellulitis, pneumonia, endocarditis and device-related infections It can also colonise the skin and nasopharynx of healthy people without causing infection MRSA is resistant to meticillin – and hence also flucloxacillin It is often resistant to other antibiotics too (multi-resistant) ``` Screening Charcoal swab (black top) Separate swabs for Nose (both nostrils) Throat (back of throat) Groin (perineum) Any wounds or device sites CSU if catheterised Different hospitals use different combinations ``` Swabs are plated onto MRSA selective agar and incubated This agar contains an indicator dye so Staph aureus colonies are green (other skin organisms will be white) It also contains antibiotics so sensitive organisms will be killed and not able to grow

Answer 35

Carbapenemase Producing Enterobacterales Enterobacterales are a group of Gram negative bacteria that live in the gut eg E coli, Klebsiella Carbapenems are very broad spectrum antibiotics that can resist most of the enzymes that bacteria produce to break down antibiotics CPE produce a carbapenemase enzyme that breaks down the carbapenem They are resistant not just to carbapenems but to most antibiotics (multi-resistant) Screening Rectal swab or stool sample Stool is better but harder to collect Red topped swab – for PCR Charcoal (black topped) swab – for culture Different hospitals ask for different numbers of swabs spaced apart (often 48 hours) This can be performed using selective agar for CPE, or by testing the sample directly using PCR or lateral flow PCR and lateral flow only look for the 5 most common genes which confer resistance There are many many more

Answer 36

risk factors Broad-spectrum antibiotic use Some more implicated than others- fluoroquinolones, cephalosporins, clindamycin Acid supressing medications (PPIs) Increasing age Hospitalisation Underlying morbidity particularly immunosuppression Inflammatory bowel disease Certain C.difficile strains more associated with severe disease- eg. type 027 Exposure to other patients with C.difficile and/or contaminated environment (including the hands of HCWs!) presentation Symptoms can range from mild self-limiting diarrhoea to pseudomembranous colitis, toxic megacolon, perforation and death Disease is caused by the toxins produced by C.difficile damaging the lining of the colon ``` Indicators of disease severity: WCC >15 Acutely rising serum creatinine (AKI) Fever >38.5 Evidence of severe colitis (clinical peritonitis, radiological changes) ```

Answer 37

INx ``` Stool sample! GDH(Glutamate dehydrogenase-antigen produced by c.difficle) PCR Toxin Interpreting the results: Not detected C.difficile CARRIER C.difficile TOXIN DETECTED ``` Management Antibiotics: Metronidazole (PO or IV) – mild-moderate disease Vancomycin (PO ONLY) – severe or recurrent disease Fidaxomicin (PO) – non life-threatening recurrent disease IVIG with combination of IV metronidazole and oral vancomycin +/- surgical management in life-threatening disease Faecal transplant in recurrent disease Prevention Address the risk factors! Antimicrobial stewardship Review of PPIs/H2-antagonists Infection control Not all risk factors are modifiable- age, hospitalisation, need for specific antibiotics Complications ``` Dehydration AKI Electrolyte Imbalance Pseudomembranous colitis Toxic megacolon Requirement for colectomy Colonic perforation Peritonitis Death ```

Answer 38

Indications Acute Urinary retention (causes-drugs,nerve injury) Bladder Outflow Obstruction-Prostatitis,blood clots Clinical unwell-fluid balance and monitering of urine output Healing of sacral and perineal wounds End of life Prolonged Immbolization-Pelvic fractures Peri operative-short term Risk factors Risk factors - Presence of urinary tract catheter! - Manipulation of catheter, trauma - Negates one of the body’s main defences against UTI: the direction of flow of urine down the urethra which helps wash out bacteria - Biofilm formation on prosthetic material: microbial cells embedded in a sticky extracellular matrix that adheres to a surface. This acts as a source of infection, and can’t be eradicated due to poor penetration of antibiotics No Catheter – No CAUTI

Answer 39

Can be difficult to diagnose: the presence of the catheter means that the patient doesn’t develop frequency or dysuria New onset or worsening of fever, rigors, altered mental status, malaise, or lethargy – with no other identified cause Flank/loin pain, pelvic discomfort, costovertebral angle tenderness Acute haematuria Risk of progressing to urosepsis NB: dark/cloudy/smelly urine can indicate dehydration rather than UTI NB: “Purple urine bag syndrome” Usually a benign condition associated with colonisation of specific bacteria (e.g. Providencia spp) Indirubin (red) and indigo (blue) are produced from metabolites of dietary tryptophan May indicate CAUTI, especially in the context of constipation INX No urine dipsticks!!! Chronic bacterial colonisation of a catheter will result in permanently positive dipstick results. This means that the dipstick results will not help with any decision-making process Urine culture, taken following TWOC/recatheterisation, or from the catheter port site (NOT the catheter bag) NB asymptomatic bacteriuria is not diagnostic – don’t treat a positive urine result in an asymptomatic patient Blood cultures (if abnormal temperature/systemically unwell)

Answer 40

Treatment Catheter removal or catheter change Antibiotics, if required: Look back at previous urine cultures to see if the patient has previous results that help inform the decision Otherwise, treat according to local antibiotic guidelines for UTI 7 days for ‘complicated UTI’ If systemically unwell: IV antibiotics for urosepsis, rationalise according to culture results Prevention Avoidance of urinary tract catheters Insertion by properly trained personnel, using good aseptic technique Unobstructed flow – no kinks in tubing, keep the bag secured below the level of the bladder to avoid backflow, empty drainage bag when necessary Encourage mobilisation, recognise and treat dehydration, resolve constipation, encourage good hygiene Removal of catheter when no longer required Routine catheter changes for long term catheters Antibiotic prophylaxis not routinely required unless significant previous infection associated with catheter manipulations Long term antibiotic prophylaxis/methenamine hippurate – not routinely advised

Answer 41

Gram positive cocci in clusters Staph aureus (MSSA and MRSA) Gram positive cocci in pairs Streptococcus pneumoniae Gram positive cocci in chains Enterococci Other streptococci (eg. Group A Strep) Gram positive rods: Clostridium perfringens Gram negative cocci: Neisseria gonorrhoea Neisseria meningitidis ``` Gram negative rods: Pseudomonas aeruginosa E.Coli Klebsiella pneumoniae Salmonella sp. Enterobacter sp. ```

Answer 42

eg. CLED agar differentiates lactose-fermenting bacteria (eg. E.Coli-yellow) from non-lactose fermenting bacteria (eg. Proteus-green)

Answer 43

E tests Combine disc diffusion and ability to generate MIC data MIC = minimum inhibitory concentration. More specific than disc testing. MICs may be useful in deciding which antibiotic to use for planned long courses for deep infections Eg we use penicillin MIC data of streptococci causing endocarditis to know when to use penicillin or amoxicillin and when to avoid them and use an alternative agent.

Answer 44

Vivax and oval-Can cause relapse

Answer 45

Sporozoites injected through human skin by female anopheline mosquito, then migrate to liver. In the hepatocytes, they multiply into merozoites. After 1-4 weeks incubation, the hepatocytes rupture and the merozoites are released into the blood. P. vivax and P. ovale can also become hypnozoites, incubating in liver for months or even years. Enter RBCs and become trophozoites then schizonts, which form further merozoites, leading to rupture and hence haemolysis and fever in 48-72 hr cycles. Some merozoites become gametocytes, which are taken up in RBCs by mosquitoes feeding on blood. P. falciparum is the most pathogenic as it affects all RBC ages, including reticulocytes, while others only affect mature RBCs

Answer 46

Epidemiology of cases imported to UK 1500 cases annually, many from those visiting family members in country of origin. Species: P. falciparum: 80%, usually Africa. P. vivax: 10%, usually South Asia. P. ovale and P. malariae: 10%. Signs and symptoms General: Fever: all tertian (48-hourly) except quartan (72-hourly) in P. malariae. These classic patterns aren't always clearly seen. Rigors Headache Diarrhoea and vomiting. Hepatosplenomegaly Falciparum malaria: Flu-like prodrome: myalgia, malaise, headache, anorexia. Irregular fever initially. Jaundice Complicated falciparum malaria: Mortality approaches 100% if severe and untreated. Cerebral malaria: altered mental status, seizures, coma, decerebrate posturing, ↑plantars, teeth-grinding. AKI Bleeding: haemoglobinuria ('blackwater fever'), DIC, retinal haemorrhages. Metabolic: ↓glucose, metabolic acidosis, Kussmaul's breathing. ARDS and pulmonary oedema. Splenic rupture. Shock

Answer 47

Diagnosis using blood films: Serial testing: up to 3 times if 1st -ve. Thick film – quick yes or no malaria – and thin film – which subtype. Also shows parasitaemia (%RBCs infected) and stage, with imminent decline in patient condition due if there are ↑schizonts. Dangerous if parasitaemia >2% and life-threatening if >5%. Simple but less sensitive antigen detection kits are available too. Immunochromographic RDT Quantitative buffy coats Antibody detection using immunoassays or fluorescence techniques Bloods: FBC: anaemia, ↓platelets. Low platelets result from increased splenic activity during haemolysis, leading to excess platelet clearance., low wbc Coag: DIC. ↓Glucose ABG: metabolic acidosis. U+E: AKI. Other tests: Urinalysis: blood. Blood cultures to rule out bacterial sepsis

Answer 48

Treatment Artemether-lumefantrine: 4 tablets then 4 tablets at 8, 24, 36, 48 and 60 h Atovaquone/proguanil (Malarone): 4 ‘standard’ tablets daily for 3 days. Quinine sulphate 600 mg 8 hourly for 5 - 7 days plus doxycycline 200 mg daily (or clindamycin 450 mg 8 hourly for pregnant women) for 7 days P. vivax, P. ovale, and P. malariae: chloroquine plus primaquine. Uncomplicated P. falciparum: 1st-line artemether/lumefantrine (Riamet). 2nd-line: quinine/doxycycline (quinine/clindamycin in kids), or atovaquone/proguanil. Complicated P. falciparum (cerebral, renal, or shock): artesunate IV (preferably), or quinine IV + doxycycline IV/PO. Careful monitoring of fluid, lactate, U+E. Transfuse if anaemic. Prophylaxis Start 1 week before to check for side effects, and continue until 4 weeks after. Areas without chloroquine resistant falciparum: Chloroquine (daily) plus proguanil (weekly). Areas with chloroquine resistance. Any 1 of: Atovaquone/proguanil (Malarone). Few side effects, and is taken from 1 day before until 7 days afterwards. Expensive. Doxycyline Mefloquine (Lariam): once weekly. Causal Directed against hepatic stage (i.e. schizonts, not hypnozoites) Prevents progression to erythrocytic stage Continue for 7 days following last possible exposure Examples – atovaquone/proguanil (Malarone) ``` Suppressive Directed against erythrocytic stages Continue for 4 weeks post-exposure Examples – chloroquine, doxycycline, mefloquine Also: ``` Long sleeves dusk till dawn. Mosquito nets DEET repellent.

Answer 49

Antimalarials Mechanism Most prevent plasmodium conversion of haem to inert haemozoin, causing toxic haem accumulation Primaquine is the only agent effective against hypnozoites. Side effects Chloroquine: headache, psychosis, retinopathy. Contraindication: epilepsy. Primaquine: epigastric pain, triggers hemolysis in G6PD deficiency (check 1st and give atovaquone/proguanil if +ve). Atovaquone/proguanil: abdo pain, nausea, dizziness. quinine-Cardiac toxicity – ECG monitoring Cinchonism-tinnitus, vertigo, N&V, visual disturbances Mefloquine: nausea, dizziness, insomnia, vivid dreams, psychosis. Contraindications: epilepsy, psychosis. Doxycycline: photosensitivity, diarrhoea, oesophagitis.

Answer 50

UNCOMPLICATED: All of the following Parasitaemia <2% No schizonts No clinical complications POTENTIALLY SEVERE: Any of the following Parasitaemia >2% Parasitaemia <2% with schizonts Parasitaemia <2% with complications SEVERE Complications present, regardless of parasitaemia

Answer 51

Leptospirosis is caused by the spirochaete Leptospira interrogans (serogroup L. icterohaemorrhagiae), classically being spread by contact with infected rat urine. Epidemiology leptospirosis is commonly seen in questions referring to sewage workers, farmers, vets or people who work in an abattoir however, on an international level, leptospirosis is far more common in the tropics so should be considered in the returning traveller Weil's disease should always be considered in high-risk patients with hepatorenal failure Features the early phase is due to bacteraemia and lasts around a week may be mild or subclinical fever flu-like symptoms subconjunctival suffusion (redness)/haemorrhage second immune phase may lead to more severe disease (Weil's disease) acute kidney injury (seen in 50% of patients) hepatitis: jaundice, hepatomegaly aseptic meningitis Investigation serology: antibodies to Leptospira develop after about 7 days PCR culture growth may take several weeks so limits usefulness in diagnosis blood and CSF samples are generally positive for the first 10 days urine cultures become positive during the second week of illness Management high-dose benzylpenicillin or doxycyclin