Leptospirosis an infectious disease. characterized by a broad spectrum of clinical manifestations (from inapparent infection to fulminant, fatal disease). Mild form: present as an influenza-like illness with headache and myalgias. Severe leptospirosis:Weil's syndrome jaundice, renal dysfunction, and hemorrhagic diathesis ETIOLOGIC AGENTS Leptospires Spirochetes order Spirochaetales family Leptospiraceae. The pathogenic leptospires are divided into serovars according to their antigenic composition. More than 200 serovars make up the 23 serogroups. Leptospires are coiled, thin, highly motile organisms with hooked ends and two periplasmic flagella that permit burrowing into tissue. 6 to 20 um long and about 0.1 um wide. Stain poorly but can be seen microscopically by dark-field examination and after silver impregnation staining. Require special media and conditions for growth; it may take weeks for cultures to become positive Morphology The Leptospira appear tighly coiled thin flexible Spritochetes Fine spiral of 0.1 – 0.2 microns One end appears bent forms a hook. Actively motile Seen best with dark field Microscopy. Greater Understanding with Electron Microscopy Electron Microscopy show thin axial filament and a delicate membrane In dark field it may appear as chain of miniature cocci. Comparative Morphology of Spritochetes EPIDEMIOLOGY Zoonosis with a worldwide distribution that affects at least 160 mammalian species

Rodents, especially rats, are the most important reservoir, although other wild mammals, dogs, fish, and birds may also harbor these microorganisms. Establish a symbiotic relationship with their host and can persist in the renal tubules for years Some serovars are associated with particular animals: icterohaemorrhagiae/copenhageni : rats Grippotyphosa: voles Hardjo:cattle Canicola :dogs pomona : pigs. Transmission May follow direct contact with: urine blood or tissue from an infected animal exposure to a contaminated environment human-to-human transmission is rare. Excreted in the urine and can survive in water for many months Water is an important vehicle in their transmission. Epidemics may result from exposure to flood waters contaminated by urine from infected animals Most commonly in the tropics because of: climate poor working and hygienic conditions favor the pathogen's survival. Certain occupational groups are at especially high risk; included are: veterinarians agricultural workers sewage workers slaughterhouse employees workers in the fishing industry Occupation Certain occupational groups such as agriculture workers in rice and cane fields, miners and sewer cleaners are potential victims Recreational exposure and domestic animal contact are also prominent sources Recreational water activities, such as canoeing, windsurfing, swimming, and waterskiing, place persons at risk for leptospirosis In a recent study in the Netherlands, 14% of patients with confirmed leptospirosis had acquired the infection while traveling in tropical countries, mostly in Southeast Asia.

Common during the rainy season in the tropics. How Man gets Infected Water the great source Drinking Swimming Bathing, as the urine of Rodents chronically infected contaminate water sources Children get infected when in contact with infected Dogs PATHOGENESIS Leptospires may enter the host through: abrasions in the skin or through intact mucous membranes (conjunctiva and the lining of the oro- and nasopharynx) Drinking of contaminated water may introduce leptospires through the mouth, throat, or esophagus. After entry of the organisms: leptospiremia develops subsequent spread to all organs. Multiplication takes place in blood and in tissues. leptospires can be isolated from blood and cerebrospinal fluid (CSF) during the first 4 to 10 days of illness. Can damage the wall of small blood vessels leading to vasculitis with leakage and extravasation of cells, including hemorrhages. The most important known pathogenic properties are adhesion to cell surfaces and cellular toxicity. Vasculitis is responsible for the most important manifestations of the disease. Mainly infect the kidneys and liver, any organ may be affected. In the kidney they migrate to the interstitium, renal tubules, and tubular lumen, causing interstitial nephritis and tubular necrosis. Hypovolemia: due to dehydration altered capillary permeability may contribute to the development of renal failure. In the liver, centrilobular necrosis with proliferation of Kupffer cells may be found Pulmonary involvement result of hemorrhage inflammation. Invasion of skeletal muscle results in swelling, and focal necrosis. In severe leptospirosis, vasculitis may ultimately impair the microcirculation and increase capillary permeability, resulting in fluid leakage and hypovolemia.

When antibodies are formed, leptospires are eliminated from all sites in the host except: the eye, the proximal renal tubules, the brain, where they may persist for weeks or months. The systemic immune response is effective in eliminating the organism but may also produce symptomatic inflammatory reactions. Meningitis: immunologic mechanism Sequence of Leptospira Infection CLINICAL MANIFESTATIONS In symptomatic cases: clinical manifestations vary from mild to serious or even fatal. More than 90% of symptomatic persons have the relatively mild and usually anicteric form of leptospirosis, with or without meningitis. Severe leptospirosis with profound jaundice (Weil's syndrome) develops in 5 to 10% of infected individuals. The incubation period is usually 1 to 2 weeks but ranges from 2 to 26 days.

Presenting with Jaundice is significant and Important, Serious Manifestation Renal failure: during the second week of illness. Hypovolemia and decreased renal perfusion contribute to the development of acute tubular necrosis with oliguria or anuria Manage by Dialysis Pulmonary involvement resulting in cough, dyspnea, chest pain, and blood-stained sputum, and sometimes in hemoptysis or even respiratory failure. Hemorrhagic manifestations are seen in Weil's syndrome: epistaxis, petechiae, purpura, and ecchymoses severe gastrointestinal bleeding and adrenal or subarachnoid hemorrhage are detected rarely. severe leptospirosis Rhabdomyolysis Hemolysis Myocarditis Pericarditis congestive heart failure cardiogenic shock adult respiratory distress syndrome multiorgan failure

LABORATORY AND RADIOLOGIC FINDINGS Related findings range from: urinary sediment changes: Leukocytes erythrocyteshyaline or granular casts) mild proteinuria in anicteric leptospirosis renal failure and azotemia in severe disease. Erythrocyte sedimentation rate (ESR) is usually elevated. In anicteric leptospirosis, peripheral leukocyte counts range from 3000 to 26,000/uL in Weil's syndrome, leukocytosis is often marked. Mild thrombocytopenia occurs in up to 50% of patients and is associated with renal failure. Elevated serum levels of bilirubin and alkaline phosphatase Mild increases (up to 200 U/L) in serum levels of aminotransferases. In Weil's syndrome, the prothrombin time may be prolonged corrected with vitamin K. Levels of creatine phosphokinase elevated during the first week of illness When a meningeal reaction develops: polymorphonuclear leukocytes predominate initially and the number of mononuclear cells increases later. The protein concentration in the CSF may be elevated CSF glucose levels are normal. DIAGNOSIS A definite diagnosis is based on: isolation of the organism from the patient rise in antibody titer in the microscopic agglutination test (MAT). Serology - ELISA Several Immunoassays are available as commercial kits Detection of IgM and razing titers of IgG will guide in association with clinical history will help in Diagnosis Leptospires can be isolated from blood and/or CSF : first 10 days of illness from urine for several weeks beginning at around 1 week. Cultures may become positive after 2 to 4 weeks. Sometimes urine cultures remain positive for months or years after the start of illness. Diagnosis of leptospirosis is confirmed: Enzyme-Linked Immunosorbent Assay (ELISA) PCR. Penicillin Drug of choice Treatment

For severe cases: intravenous administration of penicillin G, amoxicillin, ampicillin, or erythromycin. In milder cases: oral treatment with tetracycline, doxycycline, ampicillin, or amoxicillin Other antibiotics: cephalosporins, are highly active against leptospires in vitro Patients with severe leptospirosis and renal failure may require dialysis. Those with Weil's syndrome may need transfusions of whole blood and/or platelets. Intensive care may be necessary. PROGNOSIS Most patients recover. Mortality is highest among patients who are elderly and those who have Weil's syndrome. Leptospirosis during pregnancy is associated with high fetal mortality PREVENTION Individuals who may be exposed to leptospires through their occupations or their involvement in recreational water activities should be informed about the risks. Measures for controlling leptospirosis include avoidance of exposure to urine and tissues from infected animals, vaccination of animals, and rodent control. The animal vaccine used in a given area should contain the serovars known to be present in that area. Control of Leptospirosis Rodent control is most important. Human’s should avoid contact with water contaminated with animal contact. Vaccination of humans against a specific serovar prevalent in an area has been undertaken in some European and Asian countries and has proved effective. Chemoprophylaxis with doxycycline (200 mg once a week) DIALYSIS To remove fluid and uremic waste products from the body when the kidneys cannot do so Used to treat patient with edema that does not responds to treatment, hepatic coma, hyperkalemia, hypertension and uremia Acute Dialysis: indicated in high and rising level of serum potassium, fluid overload, impending pulmonary edema, acidosis, pericarditis

Chronic or maintenance: indicated in chronic renal failure,ESRD in presence of uremic signs( nausea, vomiting, severe anorexia,increasing lethargy, mental confusion) hyperkalemia, fluid overload not responsive to diuretics, fluid restriction HEMODIALYSIS Most commonly used method Favored in pts ( > 80kg) with no residual renal function. For ill and requiring short term dialysis and in pt. with ESRD 3 x a wk for atleast 3-4 hrs Components DIALYZER: synthetic semipermeable membrane/ artificial kidney, replacing glomerulus & tubules as the filter Composition and delivery of dialysate- buffer is usually bicarbonate Blood delivery system- composed of: Dialysis machine- blood pump, dialysis solution delivery system Dialysis access-fistula, graft or catheter through which blood is obtained for hemodialysis -complications include thrombosis due to intimal hyperplasia, which results to stenosis 2 to 3cm proximal to the venous anastomosis EQUIPMENT Dialyzers/ artificial kidney Flat-plate or hollow-fiber: contain thousands of tiny cellophane tubules that acts as semipermeable membrane Blood flow through the tubules while a solution(dialysate) circulate around the tubules. Exchange of wastes from the blood to the dialysate occurs through semipermeable membrane tubules Principles: Extract toxic nitrogenous substances from the blood, remove excess water Diffusion, osmosis and ultrafiltration are the principles Toxin & waste are remove by diffusion using dialysate which is made up of important electrolyte Excess water is remove by osmosis Vascular Access Subclavian, internal jugular, femoral catheters circulation for acute hemodialysis is achieved by inserting a double lumen or multilumen catheter into the access it can be used for several weeks catheter are remove when no longer needed Fistula More permanent access

Created surgically Usually in the forearm, by joining an artery to a vein, either side to side or end to side Needles are inserted to the vessels to obtain a blood flow adequate to pass through dialyser Takes 4-6 wks to mature before it is ready to use Graft Arteriovenous Created by subcutaneously interposing a biologic, semibiologic or synthetic graft material between artery and vein Used if patients vessels are not suitable for fistula, patient with compromised vascular system Usually placed in the fore artm, upper arm, or upper thigh. Infection and thrombosis are the most common complication of arteriovenous graft.

Complications during Hemodialysis Common Hypotension Muscle cramps Restless legs syndrome Nausea & vomiting Headache Chest & back pain Pruritus Fever & chills Uncommon Dialysis dysequilibrium Dialyzer reaction Arrhythmia Cardiac tamponade Intracranial bleeding Seizures Hemolysis Air embolism Long-term Complications of Hemodialysis Osteomalacia Dialysis-induced beta-2 microglobulin Myopathy Accelerated atherosclerosis, vascular calcification Hyperpigmentation Hepatitis B/C, idiopathic ascites Leukopenia, hypocomplementemia, bleeding diathesis

PERITONEAL DIALYSIS Remove toxic substances and metabolic waste and re establish normal fluid and electrolyte balance Treatment of choice for patients with renal failure who are unable or unwilling to undergo hemodialysis or renal transplantation. PRINCIPLES Peritoneum a serous membrane that covers the abdominal organs and lines the abdominal wall, serves as the semipermeable membrane The of the peritoneum constitute a body surface area of about 22, 000 cm2 Sterile dialysate fluid is introduced into the peritoneal cavity through an abdominal catheter at intervals. Urea and creatinine metabolic end products normally excreted by the kidneys are cleared from blood by diffusion and osmosis as waste products move from an area of higher concentration to an area of lower concentration across a semipermeable membrane Urea is cleared at rate of 15-20mL/min, creatinine is remove at slower rate Usually takes 36 to 48 hrs. to achieved peritoneal dialysis PROCEDURE: Preparing the patient Explain the procedure and obtains sign consent Assess anxiety, provide support and instruction Preparing Equipment cosult the Dr. to determine concentration of dialysate dialysate warmed to body temperature Assemble administration set and tubing Inserting the catheter ideally catheter is inserted in OR to maintain surgical asepsis Performing the Exchange series of cycles are involve infusion, dwell, drainage of the dialysate dialysate is infused by gravity into the peritoneal cavity period of about 5 to 10 minutes is usually required infused 2L of fluid diffusion of small molecules, urea, creatinine peaks in the 1st 5-10 minutes of dwell time Drainage is usually completed in 10 to 30 minutes Removal of excess water is achieved by using hypertonic dialysate with high dextrose concentration that creates an osmotic gradients. Complications of Peritoneal Dialysis

Catheter Pain Bleeding Leakage Poor flowPeritonitis flowPeritonitis Leakage Bleeding Hypertriglyceridemia: long term complication Acute perforation Peritonitis Nutrition High glucose, protein loss Hernia Genital edema Hydrothorax Back Pain Peritoneal fibrosis Why pts don’t live on Dialysis? *Dialysis does not replace ALL the functions of the kidneys especially those with long-term significance such as erythropoietin production and Vitamin D3 synthesis.

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