Bacteria Flashcards
Leprosy PB Treatment (first line)
6/12 Rif monthly Dapsone daily (Clofazimine also given to simplify, but this is contentious as causes darkened skin)
Leprosy MB Treatment (first line)
12/12 Rif monthly, Dapsone and Clofazimine daily
Leprosy Transmission
M leprae are found in nasal droplets of highly infected individuals and thought to enter the body through URT
Leprosy Clinical
Affinity for cooler sites of body, peripheral nerves and skin, rarely eyes, mucus membranes, testes, bones and viscera
Leprosy Incubation
Long, 3-5 years, to >20 years
Leprosy TT - CMI/bacteria
High CMI Low bacteria = PB
Leprosy LL - CMI/bacteria
Low CMI High bacteria = MB
Leprosy Borderline
At highest risk for reactions
Leprosy Skin
> 95% of patients with leprosy will have a skin lesion
Leprosy Symptoms
Numbness in hands and feet, deformities, painless ulcers or burns, nasal stuffiness, ptosis
Leprosy TT Skin
Polar tuberculoid leprosy - Well defined, asymmetrical, not many, may mimic ringworm, anaesthetic, often affecting buttocks, face and extensor surfaces of limbs (cooler parts of body)
Leprosy BT Skin
Ill defined, satellite lesions
Leprosy BB Skin
Central healing area, looks more like ring
Leprosy BL Skin
Symmetrical and more diffuse
Leprosy LL Skin
Polar lepromatous leprosy - Nodules and infiltration, associated nasal stuffiness, discharge, epistaxis, oral lesions, hoarseness. Leonine face
Leprosy Nerve signs
Thickening, dryness in hands and feet, loss of sensation in hands and feet with painless ulcers and wounds including hand burns, muscle wasting, claw hand
Leprosy Eye signs
Lagophthalmitis (inability to close eyes causes dryness), reduced corneal sensation - abrasions, acute or chronic iritis, cataract
Leprosy WHO Disability grading - Eyes
2 = reduced vision (unable to count fingers at 6m) or lagophthalmos. Nerve damage to facial and trigeminal –> lagophthalmos and/or corneal anaesthesia –> exposure keratitis and/or corneal ulcer –> blindness
Leprosy WHO Disability grading - Hands
1 = palmar sensory loss, 2= wounds, claw hand, or loss of tissue. Nerve damage to ulnar, median or radial –> loss of sensation, sweat, muscle weakness –> claw fingers and/or wrist drop –> contracture, ulceration and/or loss of digits
Leprosy WHO Disability grading - Feet
1 = sole sensory loss, 2= wounds, loss of tissue, foot drop. Nerve damage to lateral popliteal, posterior tibial –> loss of sensation, sweat and/or muscle weakness –> claw toes and/or foot drop –> contracture, ulceration, loss of digits
Leprosy Split skin
Suspected lesions, and other sites commonly affected: forehead, eyebrows, ear lobes - ZN staining and if AFB present, bacteriological index (logarithmic scale 0-6)
Leprosy Three cardinal signs
1 Definite loss of sensation in hypopigmented or reddish skin patch; 2 thickened peripheral nerve with loss of sensation/motor fx supplied by nerve; or 3 presence of AFB on slit smear
Leprosy Diagnosis
History. Full examination of skin, nerves, deformities, ulcers, wounds. Sensory testing. Voluntary Muscle Testing. Disability grading (don’t forget the eyes). Slit skin smears bacterial index/biopsy –> classification and treatment
Leprosy WHO PB Definition
5 lesions or less
Leprosy WHO MB Definition
6 lesions or more
Leprosy AE Dapsone
Hypersensitivity more common in Asia and G6PD deficiency
Leprosy AE Clofazimine
Hyperpigmentation, ichthyosis (fish scale skin) - only creates hyperpigmentation of the original lesions - associated with significant stigma
Leprosy AE Rifampicin
Orange body fluids
Leprosy PB Treatment endpoints
30% will still have active skin lesions after 6 months
Leprosy MB Treatment endpoints
BI falls 1 unit per year - look at appearances of AFBs (how broken do they look?)
Leprosy Treatment (second line)
Mino/Oflox/Clari OR monthly Rif/Moxi/Mino - newer agents Bedaquiline and Telacebec
Leprosy Chemoprophylaxis for household
Household contacts of smear positive people have increased risk of developing leprosy. WHO recommends ‘chemoprophylaxis’ with single dose Rifampicin. The Brazilian MoH recommends all household contacts be given two doses BCG
Syphilis Screening
Unless testing and treatment of syphilis in pregnancy are universally available, over half of pregnancies in women with syphilis will result in an adverse outcome
Syphilis RPR testing
Sens 85-95% Spec 95-98%
Syphilis MTCT
Primary 60%, Secondary 90%, Early latent 40%, Late latent <10%, causes 7.7% of avoidable stillbirths, although risk lower with late latent, most women are late latent, therefore most transmissions occur in asymptomatic women
Syphilis Treatment
Primary, Secondary, Early latent IM Benzathine penicillin 2.4m units stat; Late latent x3 (no evidence to support this)
Syphilis WHO elimination congenital syphilis
> 95% antenatal attenders screened, >95% seropositive treated, incidence of congenital syphilis <50 per 100,000 births
Brucella Diagnosis
GNCB intracellular on any sample inc BC, PCR, Serum agglutination ELISA >1:160 (>1:320 endemic), Rose Bengal (total Ab agglutination, not B canis)
Brucella Transmission
Low infective dose 10-100 bacteria, inhale or ingest. Commonest bacterial zoonosis worldwide - unpasteurised dairy, undercooked meat, contact with mucus membranes, aerosolisation during butchery, Lab-acquired
Brucella Epidemiology B melitensis
SE Europe, ME, Sth America, SE Asia, dairy products
Brucella Pathogenesis
Circulates in reticuloendothelial system (similar to dimorphic fungi) go to LN, bone marrow, liver/spleen
Brucella Treatment
Difficult (intracellular) Doxy 45d and Streptomycin 10d (or Gent) (relapse 5%) - second line Doxy and Rif 45d (relapse 16%)
Brucella Symptoms
Nonspecific, undulent fever (over weeks), migratory arthralgia, hepatosplenomegaly, thrombocytopaenia, elevated LFTs
Brucella Complications
Endocarditis, sacroiliitis, epididymoorchitis, OM, spondylodiscitis (Pedro Pons’ sign - erosion anterosuperior vertebrae)
Brucella Prevention
Animal vaccines, wear PPE, adequately cook meat, pasteurise dairy
Typhoid MDR, FQR & XDR Definitions
MDR: R Amp Chlor SXT, FQR: MDR+Nalidixic acid, XDR: FQR + CRO ESBL (XDR Pakistan)
Bacteriology Dental/oral common infections
Viridans - S mitis, S salivarius, S mutans, Oral anaerobes Actinomyces, Fusobacterium, S aureus
Bacteriology URT/ENT Common infections
S pneumoniae, S pyogenes, H influenzae, M pneumoniae, Moraxella sp, Chlamydia pneumophila, Fusobacterium necrophorum, N meningitidis, P aeruginosa
Bacteriology LRTI Common infections
S pneumoniae, H influenzae, M pneumoniae, L pneumophila, C pneumoniae
Bacteriology LRTI infection syndromes
COPD+Paeruginosa, Aspiration+anaerobes (Bacteroides, Fusobacterium), Zoonotic+C psittaci, Empyema+S aureus, S pneumo, S anginosus, other-Mycobacteria
Bacteriology SSTI Common infections
Staph esp S aureus, S pyogenes, Group C/G Strep, Cutibacterium, Corynebacterium, Less common B anthracis, C tetani, NTM, Nocardia sp, Vibrio vulnificus
Bacteriology SSTI Infection syndromes
Human bites+oral anaerobes, S aureus, Streps, Neisseria, Cat/Dog Bites Pasteurella (canis, multocida), Capnocytophaga, Anaerobes, Rodents+Streptobacillus moniliformis, Spirillum minus, Post-op+Pseudomonas, Enterobacterales
Bacteriology Bone and Joint Common infections
S aureus, S pyogenes, Group C/G Strep, S pneumo, N gono
Bacteriology Bone and Joint syndromes
Children: S aureus, Hib, S pyogenes, S pneumo, K kingae. Rare: Salmonella, MTB, Brucella, PJI S aureus, CNS, Corynebacterium, Pseudomonas, Enterobacterales, Cutibacterium
Bacteriology GI tract common
E coli, Shigella, Campylobacter, Klebsiella, P aeruginosa, Bacteroides fragilis, S anginosus/constellatus/intermedius, C difficile, H pylori, Salmonella
Bacteriology GI tract less common
V cholerae, L monocytogenes
Bacteriology Endocarditis
Common: S aureus, CNS, oral strep, S gallolyticus, HACEK, Enterococcus. Less common: Coxiella, Bartonella, Brucella
Bacteriology Genitourinary
Common: E coli, Klebsiella, Staph saprophyticus, Enterococcus, Proteus, S agalactiae. Others: N gonorrhoea, C trachomatis, T pallidum
Bacteriology Brain abscess
Common: Skin, dental, ear/mastoid/sinuses, lung, gut, heart valve. Others: MTB, Nocardia
Bacteriology Meningitis
N meningitidis, S pneumo, Elderly/pregnant: L monocytogenes, Unvaccinated; Hib, Neonates: GBS, L monocytogenes, E coli, Klebsiella, Serratia marcescens. CNS instrumentation: Skin flora, Pseudomonas, GNB, Others: MTB
Bacteriology Abx MOA Cytoplasm
Nitroimidazole (Metro) produce O2 free radicals which damage proteins and DNA, Lipopeptides (Dapto) depolarise cell membranes inside the cell
Bacteriology Abx MOA Chromosome
Diaminopyrimidines (Trim) interfere with folic acid synthesis. Quinolones inhibit DNA coiling. Rifampicin & Fidaxomicin inhibit RNA polymerase, Nitro causes direct damage to DNA
Bacteriology Abx MOA Cell membrane
Polymyxin bines to phospholipids disrupting cell membrane
Bacteriology Abx MOA Cell wall
Beta lactams inhibit cell wall formation, Glycopeptides (Vanc) prevent peptidoglycan cross-linkage, Fosfo binds peptidoglycan synthesis
Bacteriology Abx MOA Ribosome
Macrolides & lincosamides prevent protein elongation and inhibit ribosome formation. Aminoglycosides interfere with translation and protein formation. Tetracyclines prevent protein synthesis, Oxazolidinones prevent ribosome formation. Fusidic acid blocks elongation factor G, preventing protein formation. Chlor inhibits protein synthesis. Nitro interferes with translation
Leptospirosis Epidemiology
Global, tropical (73%) and temperate. Estimated 1 million cases and 59,000 deaths annually. 3rd most common infectious cause of life threatening disease in returning travellers. Regional variation in prevalent serovars, rainy season, flooding, hurricanes (outbreaks). Men>Women. Mortality 5-14% of confirmed cases (higher in icteric, renal failure, older)
Orientia tsutsugamushi Epidemiology
Tsutsugamushi triangle - mid Australia to Pakistan to Japan
Plague Bacteriology
Yersinia pestis, evolved from Y pseudotuberculosis 50,000 years ago
Tetanus Neonatal tetanus DDx
Neonatal tetanus (NNT), encephalitis/meningitis, rabies, TMJ disease, cerebral malaria, Strychnine poisoning
Tetanus Neonatal tetanus clinical
Risus sardonicus, trismus, opisthotonus, autonomic dysfunction (loss of preganglionic sympathetic neuron inhibition). Mortality is 68% and complications significant - microcephaly, hand-eye coordination, lower summated developmental score, neurological abnormalities and behaviour problems
Tetanus Neonatal tetanus treatment
Abx: IV penicillin +/- metronidazole. Antitoxin: human/equine, sedative: chlorpromazine/phenobarbitone. Antispasmodic: diazepam/paraldehyde. Muscle relaxant: magnesium. Reduce stimulation: quiet dark environment
Tetanus Neonatal tetanus prevention
1 Clean delivery practices (hands, delivery surfaces, cord care) 2 Tetanus toxoid protects both mother and child (unimmunised pregnant women - 2 doses tetanus toxoid 1st dose as early as possible in pregnancy, second dose at least one month later/3 weeks before delivery). 3 Infection does not provide natural immunity. WHO definition of elimination <1 case per 1000 live births in every district per year
Tetanus Localised tetanus
Contamination of wound. Presents with rigidity, pain, weakness, increased deep tendons and over weeks can progress to generalised tetanus. Mimics: Strychnine poisoning, narcotic withdrawal, hypocalcaemic tetany, neuroleptic malignant syndrome, phenothiazine dystonic reaction, rabies, stiff-person syndrome
Tetanus Cephalic tetanus
Inoculation in head. Presents with lower cranial nerve muscles, facial pain/stiffness, trismus, pharyngeal spasms, laryngeal spasms, dysphagia, neck stiffness, paresis of IX/X/III over a few days progresses to generalised tetanus
Tetanus Generalised tetanus
1 Support: Airway (tracheostomy), Muscle spasm control (benzo, chlorpromazine, vecuronium, MgSO4), Environment control (minimise light, sounds, any stimulus that can cause spasms) 2 Turn off toxin: Neutralise (human hyperimmune globulin or anti-tetanus globulin (equine)), source control (surgical debridement), antibiotic (metronidazole). 3 Complications: Autonomic dysfunction (labetalol, MgSO4 infusion), 4 Prevention: give tetanus toxoid vaccination (no natural immunity derived from infection therefore need immunisation course)
Tetanus Summary
Clostridium tetani, anaerobic Gram positive bacillus. The spores are hardy, ubiquitous environmental organisms. Tetanus toxin inhibits release of inhibitory neurotransmitters leading to uncounteracted spasms. Types: localised, neonatal, cephalic and (80%) generalised. Triad of clinical features: trismus, risus sardonicus, opisthotonos. Treatment source control, tetanus immunoglobulin, penicillin or metronidazole and supportive care. Prevention: wound care and up to date tetanus toxoid. Infection does not provide natural immunity. Maternal and neonatal tetanus elimination is defined as <1 NNT case per 1000 live births in every district per year
Trachoma SAFE
Surgery, Antibiotics, clean Faces, Environment
Yaws Epidemiology
Warm/humid environment - West Africa, South America, Pacific, SE Asia, children are main reservoir, Transmission: skin to skin contact (probably also flies)
Yaws Clinical
Primary: Painless ulcer, papilloma (golden wart >1cm nodule mostly in West Africa), resolve over a few weeks, but treponemes survive elsewhere. Secondary: disseminate, spontaneously resolve over time. Tertiary: destructive disease (tissue) no neuro/cardiac. Latent: important source of reinfection
Yaws Diagnosis
Serology TPPA (positive for life), RPR/VDRL respond to treatment
Yaws Treatment
Penicillin, also responds to Azithromycin (MDA)
Yaws Issues for elimination
Inadequate epi data, poor access to diagnostics, cost, yaws development of resistance to azithromycin, phenotypically similar to Chancroid (H ducreyi) so difficult to include/exclude as cases. Animal reservoir non-human primates
Pinta Features
T carateum, found in warm/humid environments, restricted to Latin America. Active cases in young adults are main reservoir of infection. Transmission: skin to skin
Bejel Features
T pallidum endemicum, found in dry environments (The Gulf, Sahel). Children are main reservoir. Transmission via skin to skin contact, indirect contact via utensils. Mucosal and skin lesions
Trachoma C trachomatis serovars
A-C conjunctiva, D-K urogenital, L lymphogranuloma venereum - >99% homology between ocular and genital strains
Trachoma Stages
TF (follicular) 5 or more follicles in upper tarsal, TI (intense) high bacterial load with pronounced inflammation. TS (scarring) conjunctival scarring (white lines/bands) TT (trichiasis) at least one eyelash from the upper eyelid rubs on eye. CO (corneal opacity) cause significant visual impairment
Trachoma Transmission
Flies, fomites, fingers within the family or close friends
Trachoma Treatment
Surgery (tarsal rotation), MDA Azithromycin
Trachoma Epidemiology
Centres upon Africa, with Northern South America, Middle East, South Asia (Pakistan Nepal) and SE Asia (Laos, Vietnam) also reporting cases
M ulcerans Epidemiology
Buruli ulcer, Central Africa and Southeastern Australia. Who gets disease: in Africa <15yo poor inhabitants, in Australia mostly adults. Transmission not well understood, likely inoculation by aquatic insects or mosquitos +/- ring tailed possum in Australia
M ulcerans Diagnosis
Histo on FNA or biopsy, PCR on swab , Culture too slow (can take 6 months at 32C) M ulcerans toxin likely contributes to tissue destruction through mycolactone -> cell cycle arrest, apoptosis, and downregulation of inflammatory mediators, lipid metabolism, coagulation and tissue remodelling. Histopathology demonstrates clumps of extracellular mycobacteria, subcutaneous fat necrosis, sparse inflammatory infiltrate (early, and areas of acute and chronic inflammation (including sparse mycobacteria and granulomatous inflammation - late)
M ulcerans Clinical
Non-ulcerative (papule, nodule, plaque, oedema) and ulcerative (inc osteomyelitis) - spectrum of non-ulcerative will progress to ulcerative. The ulcer will have undermined edges, and is usually painless
M ulcerans Differential diagnosis
Non-ulcer: Abscess (painful), Lipoma (mobile), Ganglion (close to joints), TB LN (constitutional sx), Onchocerciasis nodule (painless, long history), Subcutaneous infections such as fungal. Ulcer: tropical phagedenic ulcers, arterial/venous insufficiency, diabetic ulcers, sickle cell ulcer, cutaneous leishmaniasis, extensive ulcerative yaws, H ducreyi
M ulcerans Treatment
Rifampicin and Clarithromycin - no longer need surgical excision. In Aus use Rif/Moxi (not tested in RCT)
M ulcerans Paradoxical reactions
Multiple nodular lesions 2 weeks after starting abx, inflammatory reaction that prior to antibiotic treatment was suppressed by mycolactone (M ulcerans toxin), as the organisms are killed, mycolactone production ceases and its suppressive effect is lost causing a rebound of inflammation. Paradoxical response in 8.4%, lesion enlargement, pus-filled, associated with high bacterial load, heal with or without abx and/or steroids (Aus use steroids) - tends to be unpredictable
M ulcerans Complications
Cancer can develop in unstable scars years after poor healing, contracture in poorly managed wounds, amputation, eye complications, and associated psychosocial complications of mental distress, reduced quality of life, caregiver burden, stigma
M ulcerans Prevention
BCG might work (evidence lacking), mycolactone is lipid molecule that is poorly immunogenic (no vaccine possible), Control strategy - early detection, case management with appropriate abx and wound mx, prevention of disability
M ulcerans Key messages
Buruli ulcer is a NTD affecting all age groups but mainly children in Africa and elderly in Australia. Pathogenesis is mediated by a lipid-toxin mycolactone. Clinical forms comprise non ulcer and ulcerated forms. Diagnosis is mainly by PCR for M ulcerans IS2404, Treatment comprises 8 weeks of daily Rifampicin and Clarithromycin
Cholera Epidemiology
Sub-Saharan Africa, Ukraine, South Asia, ME. Increased cases in 2023 - displaced people, either within their own countries or bordering countries. Shortage of cholera vaccines - previously two doses per person, in the last 12 months have needed to reduce to one dose - preventive vaccination has stopped and is only kept for use in outbreak setting. Factors that favour cholera: Living conditions (inadequate water supply, poor sanitation, lack of personal hygiene, high population density, overcrowding) and Seasonal factors (temperature, end of dry season, rain/floods)
Cholera Pathogenesis
Gram negative comma shaped V cholerae, motile, moves at great speed in water, hides in stool of healthy and sick/convalescent. Incubation 7-10d. In endemic areas healthy carriers far outweigh the number of those unwell. Drinking water contaminated with faeces, ingest Vibrio in most cases, no Sx develop (acid in stomach acts as barrier and/or immune system is able to neutralise), but this depends on the quantity of bacteria. If it passes through the stomach, replicates in small bowel, toxin-mediated disease with rice-water stool develops. Dehydration (15L/d) - micronutrient deficiency, hypotension and death. Rehydration is mainstay of disease management rather than treating the Vibrio. Recovery occurs very fast. CFR 50% untreated, <1% with treatment
Cholera Transmission
Faeces in water to contaminated drinking water, flies, fingers (hands) soil and food
Cholera Outbreak steps
1 Defining cases: case definition 2 Confirm the diagnosis: clinical and/or biological confirmation. 3 Count cases and deaths 4 Organise the data in terms of time (epidemic curve), place (zones at risk), person (groups at risk). 5 Confirm the existence of an outbreak 6 Identify risk factors of spread 7 Analyse initial actions taken 8 Analyse information and draw up an investigation report, including feedback to persons in charge 9 Implement measures of control and prevention
Cholera Outbreak strategy
WHO Case definition “any person presenting with or dying from acute watery diarrhoea” Core problem: high mortality linked to cholera and outbreak spreading. Purpose: Cholera affected patients recover and the spread of the outbreak is limited. Data needs to be analysed daily or BD - this guides decisions and actions. Preventive activities (vaccination), community need to be involved. Treatment structures need isolation (not separate rooms, but cohorting), need to have protocols for treatment and training of staff. Early detection important as people can die within 4 hours. Decentralisation is important - be near the people within their communities as the care needs to be accessible.
Cholera Cholera treatment structures
CTC (Centre) - Completely isolated, autonomous for supplies, 24/7 max 200 beds, IV and oral rehydration. CTU (Unit) - Simpler facility, 24/7 max 30bd, IV and oral rehydration. ORP (Oral rehydration point) - outpatient, only during the day, treatment of simple cases, referral of severe cases to CTCs or CTUs
Cholera Cholera treatment protocol
Triage: Diagnosis, Initial assessment of hydration, initial po/IV hydration (ORS or ringers lactate). Hydration: Severe 10% body weight, Moderate 7.5%, Zinc supplementation for <5y, supervise every 30 min (challenging), compensate every vomit or stool. Adjuncts: Abx for severe (doxycycline), feeding, closer monitoring of pregnant or malnourished children. Print the protocol at every bed
Cholera Cholera treatment centre
4 areas: 3 for medical, 4th for staff and logistics. Chlorine is essential (inline in tanks, batch on trucks, bucket with tablets - less desirable), plastic sheeting (regularly cleaned with chlorine), beds with holes for severely dehydrated (too weak to get up), need huge quantities of chlorinated water. Chlorine used to wash beds and floor, spray feet, manage deceased. Two pronged focus: treat patients, contain outbreak. Vaccination of ‘healthy carriers’ is also important as this will reduce onward transmission. Need 15-20L water/p/d. Hygiene (hand, food, household, safe burial) Sanitation (real latrines, disposal of faeces, waste water disposal)
Cholera Cholera prevention
Vaccine - Euvichol, >=1y (including pregnant women) - 2 doses at least 14d apart (minimum interval, max interval 1y), duration of protection 6m after single dose, 3-5y after 2 doses, immunity by 7-10d after 1st dose. Single dose can cut transmission in outbreak but will not provide longterm immunity. Second dose provides more durable response. Due to shortage preemptive preventive work has stopped, currently ring strategy only (case area targeted intervention)
Cholera Cholera epidemiologic analysis
Data analysis daily in outbreak, weekly follow up, indicators used to describe the situation of the epidemic and evaluate/adapt intervention. WIR weekly incident rate, CFR, AR attack rate all used. 1 Time of death analysis useful - if there are many deaths within the first 4 hours there have been delays between the onset of symptoms and the access to treatment (distance, lack of transport, information etc) and problems in referral systems from ORP, inadequate case management and/or inappropriate waiting time in triage. Action: assess access, reinforce strategy through community education and health promotion, active early case detection, consider need to decentralise, reinforce referral systems, improve training, and adapt approach to caseload. If average length of stay is >3d need to review adherence to treatment protocols, patient monitoring, discharge criteria and presence of comorbidities. Action: Reinforce training of staff and supervision, adapt to patient workload, evaluate need of specific measures for comorbidities. Prolonged admission may reflect cause of diarrhoea other than cholera (eg HIV etc)
Leprosy Epidemiology
India accounts for 70% of cases. Unlikely accurate epi as unable to determine when infection acquired, national reporting structures unlikely to be accurate. Average time from presentation to diagnosis is 2y. Women and girls account for 40% of cases, Children <15y 5.7% (indicator of ongoing transmission), G2D are visible impairments in 5.3% of cases (indicator of delayed diagnosis)
Leprosy Differential diagnosis
Pityriasis versicolor, fungal infection, eczema, psoriasis, vasculitis, sarcoid, SLE, erysipelas, vitiligo, polyneuropathy, granulomatosis with polyangiitis, amyloid, cutaneous lymphoma, syphilis, cutaneous leishmaniasis, post-kala-azar dermal leishmaniasis, cutaneous TB
Leprosy Type 1 reaction
May occur prior to, during or after multi-drug therapy. Acute inflammation in skin, nerves or both. Typically affects pre-existing skin lesions. May be associated with facial and peripheral oedema. Nerve inflammation may lead to permanent loss of nerve function.. Immunology: M leprae antigens in skin and nerves, inflammation of tissue and/or oedema occurs. Will settle over time, but nerve can be damaged in process, difficult diagnosis to make especially if skin not involved in reaction. Treatment: Prednisolone 30-60mg/d reducing over 20 weeks, consider corticosteroid sparing agents. Summary: borderline forms of leprosy, skin and nerve inflammation, nerve function impairment, prednisolone, disability, stigma, economic hardship
Leprosy AE Corticosteroids
Lipodystrophy, Infections (esp Strongyloidiasis), Hypertension, Diabetes, Peptic ulceration, Mood disturbance, Osteoporosis, Cataract
Leprosy Type 2 reaction Erythema nodosum leprosum
May occur before, during or after multi-drug therapy. Often recurrent or chronic and is associated with morbidity, economic hardship and mortality. Debilitating multisystem disorder (fever, malaise, painful erythematous cutaneous nodules, oedema, arthritis, iridocyclitis, neuritis, nephritis, orchitis). Treatment: Prednisolone, Thalidomide (MoA uncertain but very effective). Likely immune activation, but noone has ever been able to demonstrate immune complex deposition. Summary: lepromatous leprosy, systemic disease, nerve function impairment, prednisolone, thalidomide, disability, stigma, economic hardship
Leprosy Neuropathic pain
20-30% experience neuropathic pain, many years after treatment. Nerve enlargement and tenderness are risk factors for development. Evidence of persisting neural inflammation on nerve biopsy. Exacerbates psychological morbidity, Screen patients with DN4, paracetamol/NSAID, amitriptyline, gabapentin, carbamazepine
Leprosy Compare Type 1 and 2 reactions
Both have nerve function impairment, Rx prednisolone, disability, stigma and economic hardship. Type 1 involves borderline forms of leprosy with skin and nerve inflammation. Type 2 involves lepromatous leprosy, is a systemic disease and is treated with thalidomide. All types of leprosy can get type 1 reactions, type 2 reactions occur in multibacillary disease because it is driven by bacterial antigen
Leprosy Risk factors for disability in leprosy
Delayed diagnosis and initiation of MDT. Delayed initiation of reaction treatment. Impaired nerve function at diagnosis, during and after MDT. ‘Non-adherent patients’ to prescribed MDT and supportive care. Poor mental health. Poor living conditions and poverty. Stigmatisation.
Leprosy Prevention of disability
Early detection of new cases prevents up to 30% of disabilities. Any other POD intervention during or after MDT will just prevent disability by 10%. 60% of patients may have peripheral nerve damage at diagnosis. Steroids are 50-70% effective but are ineffective if >6 months have elapsed since the most recent acute episode.
Leprosy Prevention of disability interventions
Prevention of secondary impairments: early detection and MDT before disability sets in, Mental health counselling, Early detection of nerve damage (regular NFA) - treatment and physiotherapy, quality footwear. Prevention of ‘worsening’ disability: self care practice, mental health counselling, ad hoc footwear. Reconstructive surgery
Leprosy Self care 5 components
1 Skin care (inspect daily for blisters, red spots and tender areas. Soaking for 20 min with normal water, remove hard skin with scrubber). 2 Wound care (skin trimming of the edges, dressing, health seeking behaviours) 3 Exercise (physiotherapy, active/passive exercise to prevent contractures) 4 Footwear (quality footwear, tailor made for G2D) 5 Health education (understand limitations and treatment, family support, health seeking behaviours, mental health, livelihoods). Training the patient in self-care: specific to the patient (targets disabilities they have/are at risk of), practical (the patients actually do the self-care with the health worker), achievable by the patient (promotes simple and affordable methods), repeated (to make sure that they have understood and are practicing it), empowering (the patient believes ‘I can do it’)
Leprosy Mental health
Up to 50% of people affected by leprosy suffer from mental disorders. MH issues are disabling and are a leading cause of disability worldwide. Conducting MH related interventions recognise the priorities of individuals. Mental disorders may lead to damaged self-esteem, social exclusion, lower Rx compliance, lower access to healthcare, increased disability and premature death, poverty and lower educational achievements
Leprosy Footwear
Poor footwear is the cause of 21% of ulcers. Environmental factors (occupation, rain season, culture, walking habits, previous disabilities, accidents, poor footwear) -> in setting of anaesthesia/loss of sweat (injury, deformity, increased pressure, shearing stress, skin dry/cracks) –> ulcers
Leprosy Reconstructive surgery
Most common surgeries: claw hand, foot drop, agophthalmos, decompression of nerves, wrist drop, claw toes, collapsed nose, loss of eyebrows. The application to have surgery is a long process, and patients need to demonstrate significant self-care to be eligible
Leprosy Prevention of disability summary
Early case detection. Regular nerve function assessment. Self-care practice. Mental health counselling. Quality footwear. Reconstructive surgery. Provision of rehabilitation appliances. Continuous health education. Combating stigma.
Leprosy Promoting a positive image of leprosy
New face leprosy
AMR Definition
AMR is an adaptive response to allow survival of a microbe in the face of competition from other microbes. Penicillin produced by Penicillium spp mould depletes competing bacteria, allowing the mould to flourish in that niche. Bacterial resistance to penicillin allows the bacteria to survive in a previously hostile environment
AMR Mechanisms
1 Prevent drug reaching its target (impermeable outer membrane/cell wall, efflux pump, destroy or modify the compound) 2 Alter the target (alter the target or its product so that the drug has no effect)
AMR Intrinsic vs acquired
Intrinsic: lacks antibiotic target. Acquired: point mutations - altered target, random errors during replication selected by antimicrobial pressure
AMR Transmission of resistance
Mobile genetic elements: Plasmids (circles of DNA that can move between cells) Transposons (small pieces of DNA that can go into and change the overall DNA of a cell. These can move from chromosomes [which carry all the genes essential for germ survival] to plasmids and back) Phages (viruses that attack germs and can carry DNA from germ to germ). Mobile elements and transmit via: Transduction (resistance genes can be transferred form one germ to another via phages) Conjugation (resistance genes can be transferred between germs when they connect) and Transformation (resistance genes released from nearby live or dead germs can be picked up directly by another germ)
AMR WHO monitoring
S pneumo (pen, SXT, CRO), S aureus (methicillin), E coli (amox, SXT, cip, CRO, Mero), K pneumo (SXT, Cip, CRO, Mero), Salmonella (cip, CRO, Mero), Acinetobacter (Mero, Ami, Tig, Colistin), Shigella (Cip, CRO, Azith), N gono (CRO, Azith, Spectinomycin, Cip, Gent), MTB
AMR Reduce use of antibiotics
1 Reduce disease (improve health and sanitation, vaccination, IPCU in healthcare settings) 2 reduce inappropriate use
AMR Issues in LMIC
Lack of diagnostics (lag in development of rapid bacteriology technology, ready supply of antimicrobials -> empiric treatment) Most cases of infection are managed blind to any reliable microbiological investigation. Diagnostics need to be cheaper and easier than giving an antimicrobial
AMR Empiric antibiotics
HIC: limitations on diagnosis of sepsis and causes, inherent contradiction of choosing a narrow regimen to cover a range of unknown pathogens ‘safest course is to use a broad spectrum agent’, difficult to stop or change once patient is established on a drug. LMIC: antimicrobials may be used in lieu of access to healthcare, sources may be unorthodox and unregulated
AMR AMR problems
Complicated social problem with no definite solution, no measure of success, no idealised state (approaches can only improve a situation rather than solve it), symptomatic of other problems (overuse of antimicrobials due to lack of access to clinicians/diagnostics), no definitive formulation (drivers of AMR in the UK may be grossly similar to the drivers in LMICs but discretely different (prescribing for the common cold ‘just in case’ vs prescribing for severe febrile illness in the absence of access to other healthcare/diagnostics), no clear boundaries - may impact or be impacted by other issues, no clear template for finding solutions. LMIC disproportionately suffer due to poor sanitation (increased risk of illness and increased risk of AMR transmission), more adverse consequences when infections do occur (limited access to 2nd/3rd line treatment, limited access to supportive care, poor IPCU measures increasing dissemination within healthcare settings), compounded by lack of diagnostics leading to increased use of available agents
AMR Agricultural use
Use of antimicrobials may be easier/cheaper than improving agricultural practices. Less access to diagnostics. Less information on AMR rates and antimicrobial use. Impact on human health - risk of driving AMR in animal health vs increased cost of food production and food security
AMR Measuring AMR
Rates of resistant infection (hospital and lab data), rates of resistance in carriage samples (stool screening, MRSA screening), proxy markers of resistance (environmental sampling), process indicators (antimicrobial use - point prevalence surveys, antimicrobial consumption -pharmacy records, import data)
AMR Controlling AMR
Requires multisectoral approach (prevent infection, improve antimicrobial use), cost benefit of intervention in complex health systems, tragedy of the commons (taking a broad spectrum antimicrobial may bring immediate gains to individuals now at a potential future cost to others)
Typhoid Key messages
Presentation non-specific, many people given diagnosis of typhoid do not have it, antibiotics are effective but take time to work and resistance is a problem
Typhoid Microbiology
Salmonella enterica serotype typhi, Salmonella enterica serotype paratyphi A, B & C. Gram negative bacillus. LPS antigens 09 and 012 (somatic), Hd (flagellar), polysaccharide capsular antigen Vi
Typhoid Epidemiology
India, south and SE Asia, sub-Saharan Africa
Typhoid Clinical
incubation 5-21d, fever, abdominal pain, constipation > diarrhoea, headache, cough, myalgia, neuropsychiatric manifestations. Examination: abdo tenderness (60%), hepatosplenomegaly (<40%), rose spots - little septic emboli (20%), relative bradycardia (30-50%)
Typhoid Complications
3rd week: intestinal perforation (ruptured Peyer’s patches), bleeding, sepsis, occasionally abscess. Typhoid spine - rare may occur months-years later
Typhoid Diagnosis
LMIC: only 4% of those given clinical diagnosis of enteric fever were blood culture positive. In reality, trial of treatment in pt with leukopaenia, anaemia, ALT ~400s, if diagnostics available BC or BM have good sensitivity. Widal test is serological test that lacks sensitivity and specificity - mix blood with Ag in kit, coagulation is marked as +, will be positive if previous typhoid, travellers diarrhoea and various E coli
Typhoid Treatment
Predominantly use Azithromycin at HTD regardless of country of acquisition
Typhoid Prevention
Longterm carriage (1-4%) may increase GB cancer risk. Food handling/water treatment: WASH (5Fs food, fluids, fingers, flies, faeces). Vaccines - limited protection and typhoid risk to traveller only 0.02%. Vi capsular - 1 dose 70% protection lasts 2-3y. Ty21a (oral live attenuated) - 4 doses, 60-96% protection, lasts 5-7y. Vi-rEPA or Vi-TT conjugate - 1 dose, 90% protection at 6 months. Risk in travellers low 1 in 5,000 get typhoid with mortality ~1%. need to vaccinate 500,000 to prevent one death. Vaccines should be deployed at scale in endemic regions where there are real problems with diagnosis and treatment
Plague Transmission
1 Droplet contact (coughing or sneezing on another person) 2 direct physical contact (touching an infected person, including sexual contact and unsafe burial practices) 3 Indirect contact (touching soil contamination or a contaminated surface) 4 Airborne (microorganism can remain in the air for long periods) 5 Faecal-oral (contaminated food or water sources) 6 Vector borne - carried by insects (fleas) from infected animals. The biofilm that blocks the stomach, causing the flea to starve is key to the transmission cycle
Plague Control prevention of plague
Aim to reduce likelihood of infected flea bites. To reduce direct contact with infectious tissues and exudates. To reduce respiratory exposure to pneumonic plague cases. Pest control. Flea control. Wear gloves when handling wildlife. Plague vaccine unreliable (but new developments). Fleas may remain infective for months. General susceptibility with limited acquired immunity. Variety of fleas/rodents in different places. Pneumonic cases may spread by aerosol-unusual for bubonic cases to be contagious unless direct contact with pus/discharge. Vaccines - first generation protective against bubonic but not pneumonic plague
Plague Epidemiology
Circulates in animal reservoirs, esp rodents in all continents except Australia. Foci are situated in a broad belt in the tropical and subtropical latitudes and the warmer parts of the temperate latitudes around the globe, between 55 degrees North and 40 degrees South. More than 95% of global disease reports concentrated in Africa: DRC, Madagascar, Uganda, Tanzania - however, it is reemerging in places where it had disappeared, and emerging in new locations because the natural foci of the disease are expanding. Much more sporadic in Asia - large endemic foci, but reservoir (marmots, gerbils) in less contact with humans.
Plague Vector
Xenopsylla cheopis - infection in a human generally occurs when a person is bitten by a flea that has been infected by biting an infected rodent. The bacteria multiply within flea, form biofilm plug that blocks its stomach and causes it to starve - the flea then bites a host to continue feeding, and vomits blood tainted with bacteria back into the bite wound. Bacterium then infects a new victim and the flea eventually dies from starvation
Plague Bubonic
Buboes (tender enlarged LN) smooth, tender related to the site of the flea bite. Short incubation 1-7d, may not be fluctuant or contain pus. In a fortunate few, may resolve, but mostly progress -> rapid onset of features of sepsis and dissemination including peripheral gangrene secondary to sepsis
Plague Septicaemic
Multiorgan failure/DIC -> peripheral gangrene. Bacteraemia -> severe sepsis, role of endotoxins, N&V and abdominal pain, hypotension, organ failure, DIC, localised areas of tissue and organ death (may look black), may be secondary to bubonic/pneumonic presentations or may be primary presentation. High mortality 100% in pre-antibiotic era
Plague Pneumonic
Rapidly progressive pneumonia with short incubation (2-4d), fever, weakness, nausea, then pleuritic pain, shortness of breath and cough with blood tinged sputum (containing numerous bacilli), CXR: severe pneumonia +/- mediastinal or hilar lymphadenopathy (invasion…), life threatening - high mortality. In the Johannesburg 1904 outbreak, there were detailed records and a R0 of 2-4 was calculated
Plague History
Local outbreaks of the plague are grouped into three plague pandemics, whereby the respective start and end dates and the assignment of some outbreaks to either pandemic are still subject to discussion. 541-750 spreading from Egypt to the Mediterranean and NW Europe, 1345-1840 spreading from Central Asia to the Mediterranean and Europe, probably also China, 1866-1960s spreading from China to various places, notably India and West Coast USA. All plagues were followed by labour shortages
Plague Treatment
Aminoglycosides (Streptomycin or gentamicin), Tetracyclines (doxycycline), SXT, Ciprofloxacin, Chloramphenicol.,. Macrolides don’t work, and there has never been good research into efficacy
Plague WHO Treatment
Pneumonic or septicaemic:10d Streptomycin, Gent or quinolone. Bubonic: 10d Streptomycin, Gent, Doxy or quinolone. Meningitis Moxi or chloramphenicol 10d
Plague WHO Prophylaxis
Post-exposure: 7d cipro, doxy, or SXT. Pre-exposure Doxy or SXT
Plague Diagnosis
Often missed, over-diagnosed in epidemics, tends to occur in remote settings without access to microbiology, May have neutrophilia and/or low platelet count if impending coagulopathy, but often no abnormalities are present in the pre-inflammatory phase. LN aspirate instil small volume of saline and withdraw. Blood culture, Sputum culture. Plague grows on standard micro media. Direct fluorescent antibody (DFA) or PCR can be used, esp postmortem. Madagascar have developed LFA for F1 capsular antigen to use on buboes, blood and sputum
Plague Microbiology
Growth at 22-25C is hall mark, also grows at 35C. Gram stain - bipolar GN rods with ‘safety pin’ appearance. Irregular/fried egg appearance at 48-72h.
Plague Control of cases
Report. Isolate and treat clothing and baggage to rid of fleas. Disinfection of surfaces contaminated with sputum. Disinfection and flea control in environment. Quarantine shown to be ineffective - close contacts of pneumonic cases -> chemoprophylaxis and surveillance for 7d. Investigation of contacts. Specific treatments
Plague Epidemics
Investigate all cases if possible with autopsy and lab tests. Communicate to avoid panic. Intensive flea control with insecticidal dusts. Bodies, clothing, habitats. Reduce/attack rat populations. Contact tracing and prophylaxis. Protect field workers (powder and repellents). Possibility of deliberate release an issue (most cases pneumonic? Yp live sin the air for an hour)
Plague Plasmids
pCD1 virulence factor required for infectivity. pMT1 F1 capsular Ag produces antiphagocytic slime layer. pPCP1 Pla promotes bacterial dissemination, inhibits fibrin. pCD1 type 3 secretion system, covers the bacterium in needle-like projections whose function is to inject yersinia outer proteins (Yops) into host cells, Yops induce apoptosis, inhibit phagocytosis and inhibit cytokine production and leukocyte recruitment. pMT1 encodes F1 capsular antigen that produces antiphagocytic slime layer which prevents phagocytosis (and blocks flea’s stomach), pPCP encodes plasminogen activator protease Pla which is thought to promote bacterial dissemination at the inoculation site by inhibiting the formation of a fibrin clot barrier, inhibiting innate immune cell recruitment and inactivating antimicrobial peptides
Plague Madagascar outbreaks
May have been provoked by influx of rodents (and their fleas) into human habitation following widespread bushfires and uncontrolled deforestation
Plague F1 RDT
Against culture, highly sensitive for pneumonic or bubonic plague, and can help detect plague in remote areas. Does not replace need for culture which provides additional information with AST, and genomic potential
Melioid Epidemiology
B pseudomallei GNB ox positive, environmental saprophyte. Highly seasonal, potential for long periods of latency. Endemic but underreported, greatest burden predicted to be in South Asia
Melioid Risk factors
Diabetes, renal failure, steroids, EtOH
Melioid Clinical
Variable ‘the great mimicker’
Melioid Barriers to surveillance
Very difficult to diagnose on clinical grounds alone. Affects rural poor (low priority, lack of laboratories). Lack of awareness (Doctors, Lab staff). Not mandatory notification in most endemic countries
Melioid Clinical features
Resp 40-60% (pneumonia, pulmonary abscess, pleuritis) CVS 40-60% (bacteraemia, pericarditis, mycotic aneurysm) Urinary tract 14-28% (pyelonephritis, kidney abscess, prostatic abscess) GI 10-33% (liver or splenic abscess, paraintestinal mass) SSTI 13-24% (ulcer, soft tissue abscess) Head and neck 0-30% (parotid abscess, neck abscess, lymphadenitis) MSK 4-14% (septic arthritis, myositis, osteomyelitis) CNS 1-5% (encephalomyelitis, brain abscess) Other (mastitis, mediastinal mass, corneal ulcer, epididymoorchitis, scrotal abscess)
Melioid Paediatric presentation
30% parotitis
Melioid Diagnosis
Culture is the (imperfect) gold standard (sens 60%), Serology (issues with sens/spec), PCR not routine, antigen detection.
Melioid Laboratory safety
Hazard group 3, 2 well described cases of LAI (both major lapses). No illness/seroconversion after 1267 instances of handling outside BSC. No aerosolisation during 78 routine manipulations
Melioid Antimicrobial susceptibility testing
Disc diffusion or e-test
Melioid Treatment
Minimum 2w intensive phase, followed by at least 3 months eradication phase, longer for CNS, OM and arterial infection
Melioid Biothreat potential
For: availability, intrinsic resistance, environmental persistence, high mortality, infectious by inhalation, wide host range. Against: little development of weaponisation, difficult to disseminate, ?effect in immunocompetent, no person-to-person spread. Focus on B pseudomallei as a potential agent for deliberate release undoubtedly brought benefits and funding for melioidosis as a real world health problem
Melioid Neglected
Affects rural poor, requires good laboratory to diagnose, doesn’t spread from person to person or cause explosive outbreaks
Melioid Summary
Melioidosis is any infection caused by environmental bacterium B pseudomallei. Distributed throughout tropics but grossly underdiagnosed. Predilection for diabetes mellitus. Causes sepsis, pneumonia and abscesses anywhere in body. Culture is mainstay of diagnosis. Treatment can reduce mortality from >50% to around 10%. No vaccine yet available
Orientia tsutsugamushi Clinical
Incubation 6-21d. Fever, fatigue, frontal headaches, myalgia, cough. 55% painless eschar. Delayed generalised maculopapular rash. Lymphadenopathy. Pregnancy (stillbirth, prematurity, low birth weight in >40%), mortality 1-8% (40% untreated). Immunity short lived and strain specific
Orientia tsutsugamushi Differential diagnosis
Acute febrile illness in South India: Dengue, Scrub typhus, Malaria, Leptospirosis, Typhoid
Orientia tsutsugamushi Vector
Trombiculid mite - larvae in ‘high density’ ‘mite islands’ in jungle clearings
Orientia tsutsugamushi Diagnosis
Gram negative intracellular bacteria
Orientia tsutsugamushi Pathogenesis
Widespread vasculitis and perivasculitis accompanied by infiltration of mononuclear cells into affected organs. 34% end organ failure
Orientia tsutsugamushi Treatment
Doxycycline or Azithromycin or Chloramphenicol
Orientia tsutsugamushi Prevention
Apply repellents to boots, socks, trousers, skin. Avoid sitting, lying directly on ground. For high risk people: doxycycline 200mg weekly (or daily antimalarial regimen) suppresses disease but may not prevent infection (symptoms may be postponed until after cessation of prophylaxis)
Orientia tsutsugamushi Summary
Top 5 causes of fever from South India are Dengue, Scrub Typhus, malaria, leptospirosis, typhoid. Orientia tsutsugamushi is a leading cause of treatable non-malarial febrile illness from Asia. Be aware of scrub typhus in travellers - examine thoroughly for eschars, have a low threshold to treat empirically, don’t wait for test results
Leptospirosis Biology
Spirochete, L interrogans, motile
Leptospirosis Transmission
Zoonosis: direct or indirect contact with animal [rodent] urine, leptospires survive for weeks in fresh water (less in saltwater), invade intact skin or mucous membranes
Leptospirosis Risk factors
Water or soil contaminated by animal host urine or infected animal tissue. Cuts/abrasions and inadequate footwear, water sports, mucous membranes, farming, sewerage workers
Leptospirosis Clinical
Incubation 1-30d (generally 7-14d). Early septic phase (90%): leptospiraemia, non-specific febrile illness. Complications/severe disease (10%) Immunologic phase (IgM detectable in blood, leptospire in urine) serious complications can occur including rhabdo, jaundice, AKI, pulmonary haemorrhage (>50% CFR), myocarditis, aseptic meningitis, multiorgan failure
Leptospirosis Pathophysiology
Inoculation -> haematogenous spread and dissemination -> sepsis syndrome, cytokine storm (IL6 and IL10). Severity likely related to host factors and inoculation dose (as all serovars can cause mild-severe disease). Organ damage from direct pathogen insult as well as host immune response (deranged tissue microcirculation and endothelial dysfunction, direct hepatocellular damage -> jaundice, and acute tubular damage), severe complications poorly understood but may be a form of vasculitis, haemorrhage related to endothelial damage, increased capillary fragility, thrombocytopaenia
Leptospirosis Differential diagnosis
Rickettsiae, Scrub typhus, Bacterial sepsis, Melioid, Dengue, Influenza, Hantavirus, Viral hepatitis, VHF, Malaria
Leptospirosis Lab findings
Non specific, leukocytosis, thrombocytopaenia, elevated CRP/ AKI (with hypokalaemia), elevated conjugated bili, +/- anaemia, clotting normal (no DIC). IgM (variable sens/spec - pos from d6-10, issues of cross-reactivity), PCR (blood 1st week, urine 1-3 weeks). Microscopic agglutination test (MAT) serological gold standard (MAT) available in reference centres, IgG detectable from week 2, peaks week 3-4, single titre >1:400 or 4-fold rise between acute and convalescent sera
Leptospirosis CNS leptospirosis
Lymphocytic pleocytosis (moderate, generally <500), elevated protein, normal glucose, imaging: cortical, midbrain and rarely subcortical white matter change. NB beware as can mimic viral meningoencephalitis, prognosis generally good although can have longterm sequelae
Leptospirosis Treatment
Majority mild and spontaneously resolve. Abx BenPen, CRO, Doxy, beware Jarisch-Herxheimer reaction (~9% within 24h). Supportive management: hydrate, correct electrolyte disturbances, early haemo/peritoneal dialysis, ventilation, transfusion, cardiac monitoring. No specific evidence based therapy
Leptospirosis Pregnancy
May result in fetal death, miscarriage, stillbirth or congenital lepto. Overall presentation and management the same. Consider leptospirosis early by asking about possible exposure risks
Leptospirosis Prevention
Sanitation, Shoes/protective clothing. Abx prophylaxis lacks data to support. Vaccination routine for animals, not yet for humans
Leptospirosis Summary
Common cause of febrile illness worldwide - especially in tropics/subtropics. Generally mild and spontaneously resolving. If develop complications can be fatal. If unwell enough to admit then generally given antibiotics (but consideration given to duration of symptoms at presentation). Supportive management is mainstay of treatment. Laboratory diagnosis is imperfect and requires specialist reference laboratories.
