Small group Flashcards
Yellow Fever Summary
Flavivirus. Vector: Aedes aegypti – bites different people to get a full meal, day-biting, very hardy mosquito. South America and Africa. Majority get asymptomatic disease, 20-30% will develop symptoms, most of the illnesses are self-limiting viral illness (fever, chills, myalgia), small number have severe disease with mortality 20-50% with no treatment – jaundice, haemorrhagic disease, DIC
Yellow Fever Vaccine Summary
Live. Recognised potential serious adverse events: 1 Viscerotropic yellow fever disease post-vaccination ~1/200,000 regardless of immune function. 2 - Anaphylaxis 1/1,000,000 3 - Neurotropic yellow fever disease post-vaccination ~1/200,000 and is completely reversible.
Yellow Fever Vaccine Contraindications
Contraindications: - Absolute: Immunocompromised, HIV if CD4<200, athymus. - Relative: Young infant 6-9m, pregnant and elderly(>60) 1/50,000 patients. Indications for use:
Yellow Fever Vaccine indications
Travel to endemic areas: Protecting the country not the traveller, ensuring there is no cases brought into the country
Yellow Fever Strategies
Different strategies in protecting the traveller vs programmatic vaccination vs outbreak situation. Individual: DEET, clothes covering. Vaccination in endemic countries – at the same time as MMR ~12m, if vaccine before 2yo, there is an indication for re-vaccination to make the duration lifelong. Outbreak situation: Difficult to make the vaccine, need eggs to produce, cold chain, only certain amount. Give 20% of the dose to give more people a shorter cover
Dengue Summary
Flavivirus, 4 serotypes. Vector: Aedes aegypti. Epi: Widespread along equator. Most infections are asymptomatic, some fever, rash, severe dengue thrombocytopaenia, capillary leakage. Recognised potential serious adverse events: Secondary infection with the same serotype, Antibody enhancement reaction. Third and fourth infection are usually mild. Immunity is lifelong for the serotype, so greatest risk is with the second exposure
Dengue Vaccine
Dengvaxia – single dose, YF backbone, Qdenga 2 doses, dengue backbone with cover for 4 serotypes, Countries like Brazil are trying to cover the country with vaccination
Zika Summary
Flavivirus. Vector: Aedes aegypti. Majority asymptomatic. South America Brazil outbreak of MTC with congenital disease. Prevention: avoid bites, no vaccine. If planning pregnancy: don’t travel to endemic area. Avoid pregnancy for 2m if only woman travelled, 3m if both/male partner travelled. If already pregnant: use barrier contraception. If living in an endemic country - mosquito avoidance
Diarrhoea Rainy season transmission
Possible increased transmission in rainy season: vector borne diseases where vector uses surface water for breeding (malaria, dengue). Diseases of inundation (leptospirosis). Faecal-oral transmission (risk of overwhelming sanitary facilities). Diseases of fresh water contact (Schistosomiasis)
Diarrhoea Leptospirosis Philippines
Seasonal peak during the rainy season. Thousands of people displaced and housed in emergency evacuation centres during typhoon
Diarrhoea Epidemic curves
Point source (up then down - ie hepatitis A, norovirus - vast majority of cases occur within a single incubation period), Continuous source (up then plateau ie water pump contamination). Person to person (up then down, then up with more, then down, then up with even more - although in reality, these often coalesce)
Diarrhoea Occurrence over 2 weeks period
Suggests either: a long and variable incubation period (unlikely as diarrhoeal illnesses typically have short incubations). A common, contaminated source for transmission (possible), ongoing person-to-person transmission (most likely)
Diarrhoea Stool microscopy
Inflammatory cells (red and white cells). One case has cysts of E histolytica ?significant
Diarrhoea Causes of diarrhoea with blood
Bacteria (Salmonella, Shigella, Campylobacter, E coli, Yersinia, Plesiomonas, C difficile), Protozoa (E histolytica, Balantidium coli, Malaria), Helminths (v heavy Trichuris), intestinal Schistosomiasis. Viruses (VHF esp Lassa, Marburg), Non-infectious (Inflammatory bowel disease, ischaemic colitis, radiation colitis, bowel cancer, vasculitis - all very unlikely to cause 150 cases in 2 weeks)
Diarrhoea Person-to-person spread causes
Shigella, E coli (sometimes) VHF
Diarrhoea Case management
Triage and prioritise: A send home with ORS, B at extreme risk admit, resuscitate and isolate (exclude malaria), C concerning, may be septic, resuscitate. Need an effective treatment
Diarrhoea Issues in case management
Identify high risk patients (malnourished, extremes of age, seriously ill, dehydrated, or septic), continue feeding/breastfeeding. Correct dehydration with ORS. Give an effective antimicrobial in appropriate doses. Avoid antdiarrhoeals (they are harmful), arrange to review. If an effective antimicrobial is in short supply, it may need to be reserved for high risk patients, such as those with severe or complicated disease, and milder cases managed with supportive care alone. If an effective antimicrobial is given it is reasonable to expect improvement within two days.
Diarrhoea Resistant Shigella
Resistant to all available antibiotics in LMIC except gent, however gent is typically ineffective even when Shigellae are sensitive to it, likely because of poor intracellular penetration. Quinolones such as ciprofloxacin are likely to be effective. Third generation cephalosporins (CRO) are widely used and relatively cheap (but concerns re AMS) Nalidixic acid is the cheapest quinolone regimen which is likely to be effective, but resistance has emerged rapidly under these circumstances. The story given suggests a large scale epidemic of dysentery in an LMIC setting. The main cause of these epidemics is Shigella dysenteriae type 1 which in recent years has affected Central America, South Asia and central and southern Africa. Most LMICs are at risk. The other Shigella serogroups (S flexneri, S sonnei, and S boydii), in contrast, cause milder disease are less often associated with fatal complications, are not associated with large scale epidemics and are less likely to exhibit antimicrobial resistance, although recently there has been MDR S flexneri epidemic in MSM
Diarrhoea E histolytica cysts
The finding of entamoeba cysts during episodes may lead to incorrect diagnosis and treatment. E histolytica trophozoites containing ingested RBC indicate amoebic invasion, typically amoebae do not elicit an inflammatory response and so WBCs are usually not seen in the stool in amoebic dysentery. E histolytica cysts in stool of patients with blood diarrhoea in an epidemic indicate neither that E histolytica is causing the epidemic nor that it is causing dysentery in the individual. Historically this finding led to confusion about the cause of dysentery epidemics and the treatment of dysentery cases with metronidazole which is ineffective against Sd1 and resultant continued transmission and excess mortality
Diarrhoea Shigella complications
The hazards are invasive disease leading to sepsis, dehydration (especially in children and those who are vomiting), intestinal perforation and local and remote effects of toxin (eg haemorrhagic colitis, renal failure, DIC). Febrile convulsions may occur in children. Potassium depletion may be quite severe in shigellosis, though marked dehydration is quite unusual. Hypokalaemia can be prevented by replacing faecal losses with ORS solution, and giving potassium-rich foods, such as bananas or green coconut water.
Diarrhoea HUS
Haemolytic uraemic syndrome may follow infection with Sd1 or E coli O157:H7. The classic triad of symptoms is haemolytic anaemia, thrombocytopaenia and renal failure. HUS may be mild, with rapid recovery, or severe, with kidney failure. Haemodialysis may be required if available. Clotting abnormalities can cause bleeding, and the red blood cell count may be low. Transfusions of whole blood or platelets may be needed in severe cases. With adequate treatment, many HUS patients never recovery fully. HUS should be suspected when a dysentery patient develops easy bruising and has little or no urine output. The diagnosis of HUS can be made by the following: 1 a low haematocrit 2 a blood smear showing fragmented RBC 3 a low platelet count, or platelets not seen on the blood smear, or 4 raised urea or creatinine (unavailable in many rural settings). If HUS is diagnosed, stop giving potassium-rick foods or fluids, including ORS solution, and refer the patient for hospital management if facilities are available.
Diarrhoea Shigella and E coli
Recent genomic studies suggest that shigellae should probably be classified as pathogenic strains of E coli. Extremely similar genetically. They share an invasion phenotype with EIEC. Share a large virulence plasmid Pinv A or B acquired by horizontal transfer. Shigella and EIEC evolved from the same ancestor and form a single pathovar within E coli. Biochemical differences between strains induced by minor genetic variants. Shigella strains are nonmotile as a result of minor changes - deletion in the fliF operon (flagellar coding region) or an ISI insertion mutation in the flhD operon. Shigella is an E coli…
Diarrhoea Priorities
Prevent transmission in the health centre. Educate staff and patients. Combat fear and rumour. Use local politics/structure for health education messaging.
Diarrhoea Control of Sd1 epidemics
Sd1 is an exclusively human pathogen acquired through contact with an infected case, or through eating or drinking contaminated food and water. Measures such as handwashing with soap, breastfeeding, food safety, safe drinking water, treatment of stored or piped water, safe disposal of human excreta, disinfection of clothing and safe disposal of bodies, fly screens, may be usefully promoted in health education messages. Prophylactic antimicrobials are not indicated. There is a useful document from the WHO website called ‘Guidelines for the control of Shigellosis, including epidemics due to Shigella dysenteriae type 1’
Diarrhoea VIP latrine
Ventilated improved pit latrine. Pipe doubles the cost. Flyscreen at the top, cannot get out of vent pipe. Two important features: need to be on a mound of earth so it does not flood when it rains. For the air to circulate properly, need to face the prevailing wind. Do not have a seal at the bottom and it should sink away.
Diarrhoea Water
if not fortunate, you go to the well to fill up your container of water. Water storage container can become a common contaminated source. One drop of commercial bleach can work - not enough to taste or harm people. Water and sanitation practices - modifiable and vulnerability to outbreak can be improved
Transient migratory lesions Differential diagnosis of Eosinophilia
Parasites, chronic allergy, haematological malignancy, autoimmune, vasculitidies, fungal (cocci)
Transient migratory lesions Differential diagnosis
Loa loa, gnathostoma, sparganum, another lost parasite
Transient migratory lesions Loa loa
Classically eye, Calibar swellings (esp wrists and ankles - it gets stuck at bony prominences) Geographically limited distribution: Central Africa - Equatorial Guinea, Cameroon, Central African Republic, Gabon, Congo. Transmission: Chrysops
Transient migratory lesions Gnathostoma
Ingestion of rare fish/reptiles or paratenic host. Rapid onset of symptoms. Painful hot red migratory lesions. Short and stubby worm ~2cm with a crown of spikes that can burrow through muscle tissue. Can cause eosinophilia and muscle necrosis. Global distribution
Transient migratory lesions Cutaneous larva migrans
Hook worm, including A braziliensis/A canis (zoonotic ones that get stuck in dermis of humans)
Transient migratory lesions Investigations
Filaria and gnathostoma serology, day and night bloods, US or MRI of lesion. Caution using ivermectin in loa loa endemic regions. Serology unreliable - lots of cross-reaction. Filarial films (night Wb Bm, Day Ll)
Histoplasmosis Epidemiology
Geographical distribution: East coast of Northern and South America, Sub-Saharan Africa, SE Asia, East Australia.
Histoplasmosis Diagnosis
Culture slow (need CL3 lab), Microscopy: looks like WW1 sea mines. BDG and AspAg will be positive. Serology - less useful in HIV/disseminated disease. Ag testing in blood/urine may be available. Often mistaken for TB, and can be disseminated in advanced HIV.
Histoplasmosis Treatment
Disseminated: Amphotericin. Localised, pulmonary: Itraconazole
Histoplasmosis Differential diagnosis
Talaromyces (SE Asia), Blastocystis (Nth America). In South East America, cases of histoplasmosis in advanced HIV are more common than TB
Fasciola Summary
Worldwide distribution. Zoonosis - cattle parasite (big and designed for cattle) Humans are accidental host - ingest cercariae on unwashed salad vegetables (water cress). Move through liver parenchyma causing damage, but generally not further due to large size. Acute infection: usually have eosinophilia, may have positive serology, negative OCP. Chronic infection: usually have positive serology, may have eosinophilia, intermittent eggs in stool. Treatment: triclabendazole (with buscopan and analgesia as it can be uncomfortable)
Fasciola Amoebic liver abscess
Mexico, Indian subcontinent, can cause acute dysentery, may cause an acute liver abscess. Usually circumscribed, can be massive. Rx metronidazole (melt away)
Fasciola Opisthorchis
Kazakhstan, Eastern Europe, much smaller ~1cm, much smaller operculum
Fasciola Clonorchis
East Asia, Siberia, Vietnam, SE Asia (more common) - fewer symptoms as much smaller, associated with undercooked fish
Fasciola Opisthorcis/clonorchis
Chronic biliary inflammation -> risk factor for cholangiocarcinoma (diagnosed late with very poor outcome), risk in China. Rare to present with acute symptoms as the smaller worms cause much less damage.
Mycetoma Summary
Chronic barefoot exposure, soil is packed with fungi. Microabrasions, microinoculations accumulate over a period of time. Mycetoma belt: North and South America, Central/West/East Africa, South Asia. Triad of signs: tumour (swelling), tracts, grains. Complications: disfiguring, social isolation, economically and socially disadvantages the poor. Treatment: months-to-years of Itraconazole, voriconazole (levels/monitoring challenging), surgery often ineffective (tends to relapse due to microabscesses left behind). Most ‘tropical’ diseases are diseases of poverty
Mycetoma Differential diagnosis
Madurella mycetomatis (single most common fungal cause of mycetoma), Actinomycosis (actinomycetoma), podoconiosis, TB, bacterial OM, cutaneous leishmaniasis. NTM
Malaria Diagnostics
Blood films: speciation, parasitaemia estimation. RDTs: sensitivity comparable to blood film, don’t need to be an expert, semi-speciation
Malaria Child assessment
Take ABCDE approach: A airway, B RR & SaO2, C HR BP, D GCS & signs of seizure, E check for other signs of severe malaria
Malaria Severe malaria criteria
CNS: coma/convulsions, Lungs: ARDS (adults), Respiratory distress or acidosis (children) Kidney: AKI, Shock, Hypoglycaemia (previously SE of quinine), Severe anaemia (children), Hyperparasitaemia 10% in WHO guidelines (2% in HIC settings)
Malaria Blantyre coma score
Motor: 2 localises pain, 1 withdraws from pain, 0 no/abnormal response. Verbal: 2 normal cry, 1 abnormal cry, 0 no cry. Eyes: 1 normal (tracking), 0
Malaria ACTs
ACT = Artemisinin Combination Therapy. Two (or maybe now 3) drugs in a single tablet. Main drug = an ‘artemisinin’ (artemether, artesunate, dihydroartemisinin) with combination drug = there to protect the artemisinin (mefloquine, piperaquine, lumefantrine) - first line drug for immediate treatment of all species of malaria. Artemisinins reduce parasitaemia very rapidly - everyone clears their parasitaemia by day 3. They kill more blood stages of the parasite and is probably why they are more effective. Quinine takes day 4 for 50% clearance, day 7 for complete clearance
Malaria Severe malaria features
Schizonts not usually seen in peripheral blood as is usually stuck to a capillary. If capillaries are full and schizonts leaking into blood, there is generally a severe infection. Sequestration, predominantly though to be mediated by PfEMP1 (Pf erythrocyte membrane protein) mediate binding in different parts of the body - if bind in brain -> cerebral malaria, if bind in bone marrow - anaemia, lung -> ARDS (but these are not well understood outside of brain and placenta) Malaria is more severe in first pregnancy, then slowly develop antibodies to the antigen that mediate binding to the placenta (gross simplification). Noone has ever shown that any drug that targets any of the putative mechanisms of cerebral malaria have any adjunctive benefit (and some increase mortality).
Malaria Treatment of severe
Artesunate and Ceftriaxone. Artesunate is the mainstay drug (can be given IV or rectally or IM but absorption not good). This has replaced quinine as the drug of choice. SEAQUAMAT and AQUAMAT demonstrated mortality benefit of artesunate compared with quinine. After initial artesunate switch to an ACT to finish treatment, PLUS careful fluids, strongly consider empiric antibiotics. Bacterial infections - classic association with non-typhoidal Salmonella, in severe disease often given broad spectrum Abx alongside antimalarials
Malaria Fluids
FEAST trial shows excess mortality with bolus-based fluids in children. High lactate/lowish BP is pretty common. Much of this is due to sequestration not classical hypotension. Giving fluids therefore doesn’t really help. Excess fluids plus endothelial dysfunction = BAD
Malaria Haemolysis post-artesunate
1-3 weeks after artesunate, 7-22% incidence. Haemolysis of previously infected RBC. Proportional to parasitaemia. At 2-3 week Hb check if >10%. With quinine it takes several days to work, this gives the spleen time to clear damaged RBC as opposed to artesunate - salvage more cells, but they can haemolyse later. Lose the same amount of blood with artesunate as quinine - but it happens more slowly in quinine.
Malaria HRP2 deletion
Most RDTs detect an antigen called ‘histadine rich protein 2’. This is the P falciparum specific antigen. This has generated considerable selection pressure on P falciparum > deletions of this gene are now emerging globally (ie Eritrea and Peru >20%). WHO says if ?5% should switch, btu unclear what to really do
Malaria Treatment failure
Causes: poor compliance, counterfeit drugs, drug resistance, another diagnosis. Delayed parasite clearance common in parts of SE Asia. Associated with pf13k (kelch)mutations. Increasing in Africa. This is a ‘reduced effect’ rather than a true resistance - the response slows out to the clearance time associated with quinine - the drug still works, but just need to give it for longer. What to do: treat for longer, dihydroartemisinin-piperaquine, watch out for recrudescence, triple artemisinins…
Malaria Pregnancy
WHO now recommends ACTs in pregnancy in ALL trimesters.
Malaria P vivax
Initial treatment of ALL species is with an ACT. P vivax infection -> hypnozoites in the liver. Without specific treatment these lead to recurrence. Only 2 effective drugs: primaquine and tafenoquine. Both drugs can cause haemolysis. Need to assess G6PD prior to treatment.G6PD is not a single disease, there are different levels, and if you have >30% G6PD activity then primaquine is pretty safe. Tafenoquine is long-acting primaquine - the issue is that in most parts of the world it is difficult to access G6PD level, and at least with short-acting primaquine, if someone starts haemolysing you can stop it. Study looking at clearance in high Pv setting. In those who had primaquine - 10% change of infection, in those with placebo 50% - which shows that the vast majority of vivax in this context are recurrences from liver.
Malaria Summary
Management of malaria relies on: assessment of the patient for markers of severe disease, RDTs/blood films for speciation +/- assessment of parasitaemia, ACTs are the first line drug for all individuals and all species with non-severe malaria. Artesunate (+/- antibiotics) is the first line for individuals with severe malaria. Drug resistance is emerging, esp in SE Asia. Pv and Po treatment is also needed for hypnozoites with assessment of G6PD activity. Remember you do not need to have hyperparasitaemia to have severe malaria - the percentage is just one measure of severity, don’t forget the clinical features
NTDs Assessing a child
What else would you like to know: has he received treatment elsewhere, immunisations and growth chart, is the mother well? Any other illness in the family?
NTDs Measles
Mouth: Koplik’s spots. Hepatosplenomegaly. Lymphadenopathy. Desquamating rash after measles. Complications: bacterial pneumonia, malnutrition (may be severe = Kwashiorkor), blindness. Management: Vitamin A (time to discharge and mortality significantly lower if given), antibiotics (reduced incidence of pneumonia and conjunctivitis, greater weight gain after one month). Measles mortality is 100x higher in Africa compared with Europe due to malnutrition, lack of access to care for secondary infections, overcrowding
NTDs Sickle cell
Sickle cell disease with hand-foot syndrome. Sickle crisis can cause painful necrosis of hand and feet. HbF protects from this initially, often present after 6m. Management: keep warm, analgesics, oral fluids++, antibiotics to cover S pneumo, H influenzae, non-typhoidal Salmonella, folic acid, immunisations (S pneumo, H influenzae), long term penicillin and antimalarias, education for parents. Repeated infarctions of the small bones causes significant deformity. Hydroxyurea reduces the incidence of vasoocclusive events, infections, malaria, transfusions and death in sub-Saharan Africa
NTDs TB adenitis
Painless swelling of neck, Scrofula, Diagnosis: LN aspirate and direct smear. Probably from drinking cattle milk (unpasteurised)
NTDs Congenital syphilis
Was responsible for 50% stillbirths in Mwanza, where prevalence of syphilis was about 6% in ANC attenders. Rash on palms of hands is syphilis until proven otherwise. More babies in Africa die from syphilis than those that die from HIV. Can be prevented with a single dose of benzathine penicillin delivered before third trimester. One of the most cost-effective health interventions. Symptoms: blistering rash, hepatosplenomegaly, chronic nasal discharge, palmar rash, osteitis (periosteal inflammation - responds to penicillin). Management: healthy infants born to seropositive mothers should receive benzathine penicillin 50,000 units/kg IM stat. Infants born with signs of congenital syphilis should receive procaine penicillin 50,000 units/kg daily IM x10.
NTDs Burkitt’s lymphoma
B cell lymphoma, associated with malaria and HIV. B lymphocytes proliferate to EBV, in setting of malaria T cell function is impaired, and the B cells proliferate for longer, mutation in the B cell causes the malignancy. Diagnosis confirmed by needle aspirate. Management - single dose of cyclophosphamide, vincristine and methotrexate IV, intrathecal methotrexate, beware of tumour lysis syndrome. Repeat every 2-3 weeks for at least 2 courses beyond clinical remission
NTDs Tumbu fly
Cutaneous myiasis. Vaseline suffocates the maggot - it sticks its head out, and then is removed. Prevent by ironing sheets and clothes - flies may maggots on the washing hanging on line
NTDs Cutaneous larva migrans
Hookworm - Ancylostoma canimus, self-limited. Cat and dog hookworm cannot get through the human dermis
NTDs Mycetoma (Madura foot)
Caused by either Bacteria (actinomycetes) or Fungi (Madurella mycetomatis). Starts as a painless subcutaneous nodule, progresses to multiple discharging sinuses. Black grains in the pus suggest fungal infection, red grains suggest actinomycetes. Diagnosis confirmed by microscopy or culture.
NTDs Melioidosis
Burkholderia pseudomallei, humans are infected by inoculation or contamination of wounds or mucosal surfaces by infected soil or water. Clinical features: may be a long latent period, may be localised to the lung and mimic TB, or cause osteomyelitis or abscesses in a wide variety of organs. May cause a severe sepsis syndrome with high mortality. Diabetes, renal impairment and cirrhosis are risk factors for severe disease (HIV is not). Diagnosis: culture (or serology). Treatment IV ceftazidime for 2 weeks followed by oral SXT 3-6 months
NTDs Borderline lepromatous leprosy
Treatment: Rifampicin monthly, Clofazimine 300mg monthly and 50mg daily, Dapsone 100mg daily. Patients should be warned about possible reactions and told to return immediately if they develop new neurological symptoms
NTDs Human African Trypanosomiasis
T brucei rhodesiense (acute onset, zoonosis, blood film usually positive). T brucei gambiense (insidious onset ‘sleeping sickness’, no confirmed animal reservoir, POC screening test available)
NTDs African Tick Typhus
Rickettsia africae, transmitted by cattle ticks (Amblyomma sp). Clinical features: eschar, rash (50%), regional lymphadenopathy. Diagnosis: PCR or serology. Treatment: Doxycycline 5d
NTDs Loa loa
Vector: Chrysops flies. Diagnosis: history, blood film for microfilaria. Treatment according to microfilarial load: low DEC for 3 weeks, moderate: ivermectin stat, then DEC 3 weeks. High :albendazole 3w with initial steroid cover, then DEC 3 weeks.
NTDs African Histoplasmosis
Histoplasma capsulatum var duboisii. Isolated from LN aspirate from a Belgian man in Congo with cervical and axillary lymphadenopathy. Clinical features differ from those caused by H capsulatum capsulatum - lung involvement uncommon, may cause localised or disseminated disease, characteristic skin lesions, bone an dLN commonly involved, unlike Hc capsulatum, it is not associated with HIV. In culture morphologically and antigenically identical to H capsulatum. Treatment: Itraconazole or Amphotericin, significant risk of relapsing disease.
NTDs Meningococcus
Major epidemics every few years in the ‘meningitis belt’. Always in the dry season. Can be treated with a single dose of CRO or long-acting oily chloramphenicol. Very high prevalence of nasal carriage. Traditionally caused by N meningitidis serogroup A, but recent outbreaks due to other serotypes. Conjugate vaccines are highly effective.
NTDs Leptospirosis
Zoonotic infection, many animal species infected. Caused by Spirochaetes of genus Leptospira, many species of Leptospira, each with a different animal host. Humans are infected through contact with animal urine. Bacterial can penetrate intact skin. Clinical features: Mild >90% (fever, headache, myalgia - often self-limiting), Moderate ~9% (sudden prostration, muscle tenderness, conjunctivitis, jaundice, pneumonitis), Severe (Weil’s disease, <1%) (almost always L icterohaemorrhagiae, acute hepatic and renal failure, extensive haemorrhage, myocarditis, 10% mortality). Diagnosis Spirochaetes may be seen in urine under dark field microscopy, Serology (microscopic agglutination test), PCR of blood or urine. Treatment: penicillin, amoxicillin, cephalosporins, macrolides, and tetracyclines all effective
