Morbidity and Mortality Conference

Morbidity and Mortality Conference
Jay V. Dy M.D. Medical Resident

Good Morning!

Learning Objective To present a case of Severe Leptospirosis and discuss its diagnosis, pathogenesis, complications and mode of treatment.

Identifying Data D.D. 25 year old female Filipino single
Chief Complaint: Fever

History of Present Illness
4 days PTA- undocumented intermittent fever (+) body malaise, (+) dry cough (+) sorethroat, (-) colds, rashes self-medicated with paracetamol affording temporary relief.

History of Present Illness
Few hrs PTA - persistence of symptoms (+) diarrhea, 2x (+) crampy epigastric pain (+) nausea (-) vomiting Admission (loose, watery, yellowish, non mucoid, non bloody stool. Patient went to the ER and was subsequently admitted.

Review of systems (-) headache (-) dizziness
(-) difficulty of breathing (-) orthopnea (-) paroxysmal nocturnal dyspnea (-) palpitations (-) dysuria (-) urinary frequency (-) joint pains Review of systems was unremarkable

Past Medical History Diagnosed w/ Leptospirosis 7 yrs ago
Unrecalled work up Admitted St Paul’s Hospital for several days Given unrecalled IV antibotics Non hypertensive Non diabetic Non asthmatic No known allergies No previous operation During that time, patient presented with fever, myalgia and headache. Several unrecalled labs were done and was apparently positive to Leptospirosis. Patient was given unrecalled IV antibiotics and was discharged after several days.

Family History (+) Hypertension- father (+) DM- mother
(-) Bronchial asthma (-) PTB (-) Cancer

Personal/ Social History
Non smoker Non alcoholic beverage drinker Works in the office Works in the office as a filing clerk and lives in a condo in Makati City wit her brothers.

Physical Examination General survey: conscious, coherent not in respiratory distress Vital signs: BP 110/70, HR: 98 RR: 20, T: 38c Skin: No rashes, no jaundice HEENT: pinkish palpebral conjunctivae, anicteric sclerae, no nasoaural discharge, no tonsillopharyngeal congestion, dry lips and tongue, no cervical lymphadenopathy, flat neck veins Patient’s physical examination was essentially unremarkable except for fever, dry lips and tongue and flat neck veins

Physical Examination Chest/Lungs: equal chest expansion, no retraction, clear breath sounds Heart: Adynamic precordium, normal rate, regular rhythym, S1 louder than S2 at the apex, S2 louder than S1 at the base, PMI at 5th ICS, LMCL, no murmur Abdomen: flabby, normoactive bowel sounds, soft, no tenderness, no palpable mass, no hepatosplenomegaly Extremities: no gross deformities, no edema, no cyanosis, full and equal pulses

Salient features 25 y.o, F, single cc: fever x 5 days
body malaise, dry cough, sore throat (+) 2 episodes of diarrhea (+) crampy epigastric pain (+) nausea P.E. Temp= 38c Flat neck veins Dry lips and tongue

At the E.R. Blastocystis hominis –a non pathogenic yeast and is believed by some to be a protozoan capable of causing intestinal disease. Usually not treated in asymptomatic patients. Other causes of diarrhea should be sought. But if diarrhea is prominent w/ no other attributable cause, may give metronidazole or other 5 nitro-imidazole like secnidazole

Day of Admission Chest xray was normal

Initial Impression Acute gastroenteritis with some signs of dehydration T/C Dengue fever

Course in the Wards 1st hospital day (8/3)
intermittent fever (D6) (Tmax c) bloatedness crampy epigastric pain diarrhea, 8x vomiting, 1x Secnidazole 500mg/tab. 4 tabs as single dose Metoclopramide 10 mg Iv push q8 Loperamide 2 tabs x 1 dose IVF rate: increased to 166 cc/hr. Secnidazole- is a 5-nitroimidazole which has a high antiparasitic effect against a wide variety of anaerobic protozoal parasites and bacteria. Blastocystis hominis –a non pathogenic yeast and is believed by some to be a protozoan capable of causing intestinal disease. Usually not treated in asymptomatic patients. Other causes of diarrhea should be sought. But if diarrhea is prominent w/ no other attributable cause, may give metronidazole or other 5 nitro-imidazole like secnidazole

Course in the Wards 1st hospital day (8/3)
PTT (n.v secs) PT was normal plt ct 69,000 from 109,000 > Monitoring of platelet ct q 12 hrs. >Stand by 4 units of FFP PTT was elevated at There was further decrease in platelet count. There were no any signs of bleeding at this point like gumbleeding or osebleeding. Fresh frozen plasma contains stable coagulation factors and plasma proteins (fibrinogen, antithrombin, albumin, prot c&s). INDICATIONS for FFP: correction of coagulopathies, rapid reversal of warfarin, TTP PTT & PTT assess plasma coagulation function. PTT screens the intrinsic limb of the coag system and tests for the adequacy of factors VII, IX, XI, XII……. PT screens the extrinsic or tissue dependent pathway

2nd hospital day (8/4) on and off fever (D7) (37.0- 39.5 c)
bloatedness crampy epigastric pain 7 episodes of LBM 3 episodes of vomiting direct epigastric tenderness Plain film of the abdomen: no localizing signs hydration/meds were continued additional dose of Loperamide and Eldicet started Vamin glucose

2ND Hosp day PFA: No localizing signs

Course in the Wards 2nd hospital day (8/4)
Lab test K BUN creatinine K correction was given. (kcl drip: 100cc pnss+30 meqs kcl x 4 hrs for 2 doses) Accurate Input and output monitoring and rpt electrolytes were requested

Problem: (+) Difficulty of breathing Respiratory rate: 26 Flat neck veins Clear breath sounds ABG: uncompensated metabolic acidosis. pO2=96.9, pH=7.28, Pco2=20.1, HCO3=9.3, O2 sat=96.8, B.E.-14.9, Total CO2=9.9, RR=26, Rm air given NaHCO3 IV Metabolic acidosis: can be due to 1) diarrhea (loss of bicarbonate) 2) renal failure (accumulation of endogenous acids) Anion gap (nv mmol/l) formula: AG=[Na] - (Cl + hco3) -represents those unmeasured anions (anionic proteins, sulfate,and organic ions) in plasma An INCREASE in AG may be due to a decrease in unmeasured cations (Ca, Mg, K) or an increase in unmeasured anions

2nd hosp day (aug4) Chest xray: NORMAL

CBC: Hgb 8.2, hct 23.6, seg 8,320, seg 77, lym 17 and plt ct 71,000 >Reserved 2 u prbc >repeat CBC w/ plt ct in am >Blood culture done >Referred to Nephrology & Infectious disease service Noted to have anemia with a hgb 8.2 from PLt ct 71,000 fro 64,000.

3rd hospital day (8/5) (+) fever (D8) (Tmax39.6 c)
(+) Epigastric tenderness (+) decreased BM (semi-formed to soft) (-) vomiting Rpt CBC: Hgb 8.4, hct 24.4, plt ct 84,000 from71,000 Transfused 1 of 2 unit Prbc Increased omeprazole to 1 cap BID

Course in the Wards 3rd hospital day (8/5)
PTT PT: Activity 66.4% INR 1.2 Vitamin K given Urinalysis showed proteinuria +2, Blood +3, elev RBC 572.2, elev WBC 14.4 Urine CS requested

3rd hospital day Problem: (+) dyspnea (+) distended neck veins
(+) bibasal crackles (+) bipedal edema Lasix 40mg IV given IVF rate was decreased to 40cc/hr Central line inserted (13-14 cmH2O)

2nd hosp day rd hosp day

3rd hospital day (8/5) Stat ABG: Po , Ph 7.27, Pco , HCO , O2 sat 83,B.E. -10.9, TCO2 15.7, RR 28 (O2 2LPM via Nasal cannula). > Nasal cannula was shifted to MVM > stand by intubation > scheduled for stat Hemodialysis

Spec (pre HD) K 2.7, Ca 1.5, total protein and Albumin 1.6 bun 23, crea 3.1, SGOT 336, SGPT 78 and T. Bili 1.4. Given K, Ca, and albumin correction

During dialysis: transfused w/ 4 units FFP (150cc/unit/bag)=600cc 1 unit Prbc (250cc) 550cc flushing/ meds Na HCO3 40 cc/hr x 4 hrs= 160cc Ca Gluconate 80 cc/hr x 4 hrs= 320cc Kcl drip 10% 40meqs x 4 hrs = 100cc UF Volume (output)=4,000 cc HD total Input= 1,980 cc

3RD hosp day (Aug 5)

> scheduled for another hemodialysis. > Total Input=3,910 cc vs Total output=4,340 cc (urine HD 4,000cc)

Leptospira antigen test:(+) IgM
> Penicillin G 2 million units IV q 4 given.

4th hospital day (8/6) Problem: dyspnea BP: 110/60; CR 120s; RR40s
decreased urine output (7-8 cc/hr) (+) bloody secretions/sputum. CVP 15 cmH2O ABG: Po2 39, ph 7.41, Pco2 32.9, HCO3 20.6, O2 sat 75.1, B.E. -3.0, TCO2 21.6, RR 60 MVM 0.4 reffered to a pulmonologist

Course in the Wards 4th hospital day (8/6)
immediately intubated hooked to a mechanical ventilator (settings: AC mode, FiO2 100%, RR 20, TV 300, PEEP 5).

post intubation

ABG 1 hr post intubation still showed hypoxemia (pO2 58, O2 sat 91
Atrovent neb given PEEP was increased to 7.5 Patient immediately underwent (2nd)hemodialysis

Pre HD Labs decreased serum K (2.4 from 2.7), Ca 1.9, Phosphorus 2.3 and Mg 1.6 ( ). Serum creatinine further increased (4.6 from 3.1) Patient was given K, Ca, Mg and phosphorus correction

During dialysis: 100cc flushing/ meds PNSS 40 cc/hr x 4 hrs= 160cc Vamin glucose 40 cc/hr x 4 hrs= 160cc Albumin 50cc HD total Input= 470 cc UF Volume (output)=3,000 cc

afebrile (+) tachycardia ( ) (+) decreased urine output (4-5cc/hr) JVP 13cmH2O Lasix was continued

Post Intubation 5th Hosp day

Patient underwent 3rd hemodialysis. During dialysis: 50cc flushing/ meds K Phos 40mmol in PNSS 100ccx 4hrs= 100cc Ca Gluc 5 g in 450cc pnss x 20cc/hr x 4=80cc MgSO4 5 g in 500cc PNSS X 20cc/hr x 4=80cc total Input= 470 cc UF Volume (output)=2,000 cc

Pulmonary service was able to bring down FiO2 to 0.6 but had desaturation eventually placed back to 100% FiO2 More bloody secretions coming out/ suctioned from ET Frequent/ prn suctioning of secretions. PEEP was increased to 10.

CBC: Hgb 12.1, hct 35.1, wbc (15, 760 from 6,850), seg 74, plt ct 135,000 fro 128,000). Pen G was discontinued Piperacillin Tazobactam 2.25 IV q8 was started. Total Input: 2,298cc Total Output: 2,107cc (Urine 107 cc+ HD 2,000cc)

afebrile (D2) lesser bloody secretions from ET. Persistent oliguria (4-5 cc/hr) Lasix was continued patient had another dialysis (4th)

During dialysis: 50cc flushing 100cc OF Ca Gluc 5 g in 450cc pnss x 20cc/hr x 4=80cc Dialysis terminated due to BP 94/63 (3rd hr) Bp went up 110/70 after total Input= 230 cc UF Volume (output)=1,700 cc

chest xray post HD: clearing of bilateral lung infiltrates. FiO2 was titrated down to 30%.

S/P 4th dialysis

Problem: desaturation (02 sat 50%). Fi0 was increased to 100% suctioning of secretions ambubagging BP noted to be 0, HR 0. hooked to a cardiac monitor: flat line. CPR done Given epinephrine 1 dose

revived after 3 minutes Dopamine drip was started. Bp went up to 110/70 from 50 pallpatory ABG: mixed (slight) metabolic and respiratory acidosis with PO2 496 at FiO2 1. Patient became fully awake and responsive

30 mins after referred again (O2 desaturation 80%) suctioned secretions BP=0, HR=0, flat line on cardiac monitor CPR was done but after 15 minutes, relatives ordered to discontinue CPR Patient was then declared expired.

Problem #1 Fever/Diarrhea
S> DOA: (+) Fever, (+) diarrhea (+) myalgia (+) nausea/ vomiting/ epigastric pain (+) dec platelet ct. 69,000 from ,000 O> Temp= 38c flat neck veins Dry lips and tongue

Problem #1 Fever/Diarrhea
A> T/C Dengue fever; > Acute gastroenteritis with some signs of dehydration > R/O Typhoid fever P> Plasil 10 mg IV q 8 for vomiting Loperamide tab Ciprofloxacin 500mg tab bid Secnidazole tab 4 tabs x 1 dos Hydration IVF platelet ct monitoring q12 Blood CS

Problem #1 Persistent fever
S> 3rd hospital day: (+) fever (D8) (+) wading in floodwater 3wks (+) Myalgia before onset of fever (+) nausea (+) decreased urine output/ elevated crea 3.1 (+) elevated SGOT 336 O> temp 38.5c A> T/C Leptospirosis P> Leptospira Igm (+) Penicillin G 2 million units IV q4

Problem #1 Persistent fever T/C Typhoid fever
Points for Prolonged fever (75%) Abdominal pain (20-40%) Diarrhea (30-50%) Non specific symptom (myalgia, nausea) Points against >No rash (rose spots) (30%) >No response to Ciprofloxacin despite 3 days tx >Negative Blood Culture (60-90% yield)

Problem #1 Persistent fever Malaria
Points for >Fever spikes Points Against No history of travel to endemic areas Prominent diarrhea and abdominal pain suggests another dx >non specific symptoms (no headache, chills)

Fever pattern

Problem # 2 Decreased urine output
Oral/ OF Parenteral Total Input Urine Crea BM Dialysis output DOA 1,660 1,640 3,300 9x 1st HD 3,325 6,625 13x 8x 2ndHD 2,260 4,620 6,880 3.1 7x 3rdHD 1,090 2,820 3,910 340 2x 4,000 4,340 4thHD 810 1008 2,933 78 4.6 1x 3,000 3,078 5thHD 673 1625 2,298 107 3.8 2,000 2,107 6thHD 460 568 1,028 33 1,700 1,733

Problem # 2 Decreased urine output
O> JVP 6-7cm H2O > JVP cm H2O Clear breath sounds---->Bibasal crackles (-) edema >grade 2 bipedal edema A> Acute renal failure probably pre renal 2 to dehydration (GI fluid loss) and/or Intrinsic renal failure secondary to leptospirosis P> accurate I & O monitoring monitor bun, crea, electrolytes hydration< >hemodialysis

2nd HD 3RD HD 4TH HD 5TH HD Na 135 140 132 K 2.3 2.7 2.4 2.9 BUN
mmol/L 135 140 132 K mmol/L 2.3 2.7 2.4 2.9 BUN mmol/L 23 (8.3) 37 (13.2) 31 (11) Crea 53-88 Umol/L 3.1 (274) 4.6 (406.6) 3.8 (335)

Problem # 3 Difficulty of Breathing
S> (+) Difficulty of breathing (+)bloody secretions urine output: 340cc/24 hrs(14cc/hr) total input:4,490cc/24 hrs(187cc/hr O> RR=40s (+) distended neck veins (+) bibasal crackles (+) bipedal edema

A> Acute Respiratory failure 2 to Pulmonary congestion probably secondary to Acute renal failure

2nd hosp day Day of Adm

3rd hosp day 3rd hosp day

4th Hosp day 5th Hosp day

6th Hosp day Post dialysis 5th Hosp day

P> Nasal cannula was shifted to MVM > stand by intubation--Intubated > Hemodialysis > NaHCO3 IV > CVP monitoring > Accurate I & O

Problem# 4 Hypokalemia S> (+) diarrhea x several episodes
(+) vomiting x several episodes A> Hypokalemia probably 2 to GI loss (diarrhea) P> Na, k, crea monitoring KCL drip urinary K excretion- not done

Problem #5 ANEMIA S> (+) bloody/frothy secretions suctioned per ET
(-) black stools/ bloody stools O> pale palpebral conjunctivae (-) Petechiae (-) bruises

Hgb Hct RBC WBC Seg Lym Mon Plt ct DOA 1st HD 2ndHD 3rdHD AM 3RDHD PM
5THHD 6THHD Hgb 12.1 10.5 8.2 8.4 14.8 10.4 Hct 35.5 30.8 23.6 24.4 42.3 35.1 30.2 RBC 4.3 3.8 2.9 3 5.3 4.4 WBC 13,470 7,960 8,320 6,850 15,650 15,760 16,580 Seg 91 80 77 79 76 74 75 Lym 6 18 17 15 14 Mon 2 4 9 10 Plt ct 109,000 69,000 71,000 84,000 128,000 135,000 180,000

Problem #5 ANEMIA A> Anemia probably secondary to acute blood loss
(T/C Alveolar /Interstitial hemmorhage) T/C Anemia secondary to renal failure T/C Anemia secondary to Sepsis P> CBC monitoring Blood transfusion(2 u prbc) PT/PTT- prolonged PTT (49.6) Peripheral smear: rbc: normocytic, normochromic, pletelets: decreased PERIPHERAL SMEAR: can provide important information as to the presence and nature of erythropoeitic defect Reticulocyte count (nv 1-2): percent of newborn rbcs in the circulating red cell population. Elevated retic ct provide a reliable measure of rbc production in response to anemia. CBC and reticulocyte index are used to intially classify an anemia as either hypoproloferative (a maturation disorder) if (<2) or hemolytic/ hemorrhagic anemia If (>3).

DIAGNOSIS #1 Severe Sepsis (Leptosprosis)
#2 Acute renal failure probably Intrinsic and pre renal secondary to leptospirosis and dehydration (GI fluid loss) #3 Acute respiratory failure 2 to #2 #4 Anemia probably secondary to alveolar hemorrhage, renal failure and Sepsis #5 Hypokalemia secondary to GI loss (diarrhea) Severe sepsis: sepsis with 1 or more signs of organ dysfunction, hypoperfusion or hypotension, such a metabolic acidosis,oliguria/anuria

Cause of Death ? Mucus Plug Septic Shock Arrhythmia Hypokalemia
Pulmonary Embolism

Cause of Death ? Points For Points Against Mucus plug Sudden dyspnea
Sudden O2 desaturation (+) mucus plugs/ big blood clots on the tip and inside the lumen of the Endotracheal tube upon removal Septic Shock Elevated WBC count 16,580 from as low as 6,850 Tachycardia (+) Leptospira IgM Had O2 desaturation first before BP went down Septic shock: sepsis with hypotension that is unresponsive to fluid resuscitation plus organ dysfunction Severe sepsis: sepsis with 1 or more signs of organ dysfunction, hypoperfusion or hypotension, such a metabolic acidosis,oliguria/anuria

Cause of Death ? Points For Points Against Arryhthmia/ Hypokalemia
Cardiac monitor: showed no arrythmia Improving K level (2.9 from 2.4) w/ ongoing correction Pulmonary Embolism Sudden onset dyspnea, O2 desaturation, tachycardia, Patient is relatively immobile (intubated) pO2 400

CASE DISCUSSION Leptospirosis

Leptospirosis zoonosis with protean manifestations
caused by the spirochete, Leptospira interrogans

Infection in small rodents (carrier animals) usually occurs during infancy
animals shed the organism in their urine intermittently or continuously throughout life resulting in contamination of the environment, particularly water. Organisms may remain viable for days to months in soil and water with a neutral pH.

Portals of entry include cuts or abraded skin, mucous membranes or conjunctiva. The infection is rarely acquired by ingestion of food contaminated with urine or via aerosols. Controversy exists as to whether Leptospira can penetrate the intact skin.

Risk factors for infection
Occupational exposure — farmers, ranchers, abattoir workers, trappers, veterinarians, loggers, sewer workers, rice field workers, military personnel, laboratory workers Recreational activities — fresh water swimming, canoeing, kayaking, trail biking

Household exposure — pet dogs, domesticated livestock, rainwater catchment systems, and infestation by infected rodents. Other — Skin lesions, contact with wild rodents

The spirochetes enter the host through abraded skin or intact mucous membranes and travel to the liver where they reproduce. After an incubation period of 2 to 30 days (usually 5 to 14 days), leptospiremia occurs, spreading organisms to all parts of the body including the meninges

LEPTOSPIROSIS 2 general patterns occur:
1 anicteric leptospirosis (90%) 2 icteric leptospirosis or Weil disease (10%)

CLINICAL MANIFESTATIONS
fever (75 to 100) Myalgias (50-80%) headache (15-30%) nonproductive cough (25 to 35%) nausea, vomiting and diarrhea (50%)

less common symptoms: arthralgias bone pain sore throat abdominal pain

Physical examination conjunctival suffusion- (40-70%) muscle tenderness (30-40%) Jaundice (50-80% in severe form) Splenomegaly Lymphadenopathy Pharyngitis Hepatomegaly skin rash

Liver failure is generally reversible and not a cause of death in leptospirosis.
Dyspnea, oliguria, WBC counts above 12,900/mm3 Alveolar infiltrates on chest radiography have been associated with adverse outcomes.

Complications — While most cases of leptospirosis are mild to moderate, the course may be complicated by renal failure, uveitis, hemorrhage, acute respiratory distress syndrome, myocarditis and rhabdomyolysis

The potential severity of leptospirosis was illustrated in a retrospective study of 60 patients with leptospirosis requiring ICU admission in India . Multiorgan failure developed in 46 patients (77 percent) the mortality for patients with leptospirosis requiring ICU admission was 52 percent.

Severe pulmonary disease may be underdiagnosed in regions of high endemicity.
Among 321 patients with serologic and clinical evidence of leptospirosis in Peru, seven (3.7 percent) had severe pulmonary manifestations, including hemoptysis in six 5 of the 7 patients died, 4 from pulmonary hemorrhage and 1 from acute respiratory distress syndrome and multiorgan failure

LABORATORY FINDINGS — Leptospirosis is a nonspecific clinical illness, and routine laboratory tests are similarly nondiagnostic. White blood cell (WBC) counts are generally less than 10,000/mm3 but may range between 3,000 and 26,000/µL Urinalysis frequently shows proteinuria, pyuria, granular casts and occasionally microscopic hematuria Elevated creatine kinase is found in approximately 50 percent of patients and may be a useful clue for the diagnosis

Approximately 40 percent of patients have minimal to moderate elevations of hepatic transaminases (usually <200 IU/L). Hyponatremia is common in severe leptospirosis.

Thrombocytopenia is uncommon, but a poorly understood hemorrhagic diathesis may occur in the absence of demonstrable coagulation defects or severe thrombocytopenia. Pancytopenia has been reported as the presenting manifestation in case reports with complete resolution following treatment with penicillin [29]. The CSF may show a neutrophilic or lymphocytic pleocytosis with minimal to moderately elevated protein concentrations and normal glucose. A low CSF glucose concentration is rarely seen [30].

Imaging — Chest radiographs may show small nodular densities, which can progress to confluent consolidation or a ground glass appearance Pathologically, these infiltrates may represent alveolar hemorrhage, ARDS, or pulmonary edema

DIAGNOSIS — Because the clinical features and routine laboratory findings of leptospirosis are not specific, a high index of suspicion must be maintained for the diagnosis. The organism can be cultured, but the diagnosis is more frequently made by serologic testing.

Culture — As noted above, leptospirosis can be confirmed by culture of the organism from clinical specimens in appropriate media. B Blood and CSF specimens are positive during the first 10 days of the illness. I Isolation of the organism from the blood is successful in approximately 50 percent of cases. Urine cultures become positive during the second week of the illness and remain so for up to 30 days after the resolution of symptoms

Serology — Because some clinical microbiology laboratories do not offer culture for the diagnosis of leptospirosis, serological tests are most often used for confirmation. A number of serologic tests are employed or are under development, including the microscopic agglutination test (MAT), macroscopic agglutination test, indirect hemagglutination, and ELISA

While all of these assays are useful in establishing the diagnosis, the gold standard is considered to be the MAT Unfortunately, this test requires live organisms, considerable expertise, and is performed only by reference laboratories such as the CDC. Like other serologic tests, the MAT is most specific when a fourfold or greater rise in titer is detected between acute and convalescent serum specimens. However, a single titer of >1:800 is strong evidence of current or recent infection with leptospira.

Cross reactive antibodies have been associated with syphilis, relapsing fever, Lyme disease, and legionellosis [1]. The level of the antibody titers as found in the MAT cannot be used to predict the serovar that infects the individual patient

Since the MAT is not readily available, another assay typically is performed first in suspected cases of leptospirosis. Two commercially available rapid tests, the microplate IgM ELISA and an IgM dot-ELISA dipstick test, performed well in studies conducted in the United States and Thailand that used MAT as the comparator If one of these assays is positive, sera for MAT can then be sent to the CDC

LEPTOCHECK (Rapid test for antibodies to Leptospira)
Sensitivity 100% (only 90% in a study made in India by Maskey et at) Specificity 92% (Maskey et at)

TREATMENT — The vast majority of infections with leptospira are self-limiting.
Although penicillins, tetracyclines, chloramphenicol, and erythromycin have anti leptospiral activity in vitro and in animal models, it remains controversial whether antimicrobials produce a beneficial effect in mild human leptospirosis since the illness has a variable natural history.

Nevertheless, if the illness is severe enough to result in a physician visit and the diagnosis is recognized, antibiotic therapy should be given.

Efficacy — Two small, randomized, placebo-controlled trials have shown a benefit from antimicrobial therapy. In one in which doxycycline (100 mg PO twice daily) was compared to placebo, doxycycline shortened the illness by an average of two days and prevented shedding of the organism in the urine [1].

In the second trial, patients with severe leptospirosis who were treated with penicillin (6 million units daily) had fewer days of fever, more rapid resolution of serum creatinine elevations, and a shorter hospital stay; penicillin therapy also prevented urinary shedding

Supportive care with dialysis, ventilatory support, and blood products may be necessary in severe cases of leptospirosis. Antimicrobial treatment — Human leptospirosis is often self-limited and requires no antibiotic treatment. Symptomatic patients presenting for medical care should be treated to shorten the illness and decrease shedding of the organism in the urine. We suggest the following approach that varies with the clinical presentation

We suggest treatment with oral doxycycline for outpatients because it is also effective for rickettsial disease, which can be confused with leptospirosis (100 mg orally twice daily in adults; 2 mg/kg per day in two equally divided doses in children 8 years of age to a maximum dose of 200 mg daily).

The exceptions are children 8 years or pregnant women, in whom we suggest treatment with amoxicillin (25 to 50 mg/kg in three equally divided doses).

For hospitalized adults with severe disease, we suggest intravenous therapy with penicillin (6 million units daily), doxycycline (100 mg twice daily), ceftriaxone (1 g every 24 hours), or cefotaxime (1 g every six hours).

PROGNOSIS — Mortality rates in hospitalized patients with leptospirosis have ranged from 4 to 50 percent. Pulmonary hemorrhage (30-70%) A retrospective review of 282 cases of leptospirosis during a 2002 outbreak in India identified risk factors for mortality

Most authorities agree that if antibiotics are not started early in the disease (up to the fourth day), they do not change the course of the illness (50-80%motality)

PREVENTION — Vaccination of domestic animals against leptospirosis provides substantial protection, but is not effective in 100 percent of animals. Some immunized animals become infected and excrete leptospires in their urine.

The major control measure available for humans is to avoid potential sources of infection such as stagnant water, water derived from run off from animal farms, rodent control, and protection of food from animal contamination.

Thank you

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