Leptospirosis

LEPTOSPIROSIS

OBJECTIVES

• GENERAL:– To present a case and discuss about

Leptospirosis

• SPECIFIC– To discuss the incidence and epidemiology

of the disease– To discuss the pathophysiology of

Leptospirosis– To discuss the complications of the

disease– To discuss the guidelines in management

and treatment of leptospirosis– To discuss the prevention of the disease

GENERAL DATA

This is a case of M.F. 59 y/o male, married, Filipino, Roman Catholic, born on October 13, 1954, presently residing at 04 Capoas St. Masambong Quezon City admitted at QCGH on September 15,2014

CHIEF COMPLAINT

DIFFICULTY OF BREATHING

HISTORY OF PRESENT ILLNESS

• 3 months prior to admission patient had history of flood wading.

• 2 months prior to admission patient had febrile episodes associated with myalgia

• 1 week prior to admission he sought consult at QCGH ER, was diagnosed with UTI and given ceftriaxone

HISTORY OF PRESENT ILLNESS

• 4 days prior to admission patient experienced easy fatigability with decreased urine output

• 1 day PTA patient sought consult again for generalized body weakness, advised admission but went HAMA

• On the day of consultation patient developed difficulty of breathing

PAST MEDICAL HISTORY

• Unremarkable

Comorbidities?History of previous infection?

FAMILY HISTORY

• Unremarkable

Family members with history of leptospirosis

PERSONAL AND SOCIAL

• Smoker with 5 pack years• Heavy alcoholic beverage drinker

Description of the patient’s residenceEnvironment and community?Work of the patient?Vectors in the area?Incidence of floods?

REVIEW OF SYSTEMS

• Head and Neck: No headache, injury, neck stiffness

• Ears: No changes in hearing, otalgia, tinnitus, ear discharge

• Nose: No colds/nasal stiffness, bleeding, dryness, discharge, pain, sneezing

• Mouth/Throat no bleeding gums, soreness, ulcer, hoarseness, pain, dryness, difficulty in swallowing

REVIEW OF SYSTEMS

• Hematology no bruises, pallor• Endocrine no heat or cold

intolerance, polyphagia, polydypsia, polyuria

PHYSICAL EXAMINATION

GENERAL: Patient is, conscious, coherent, non ambulatory,in severe Cardio Repiratory Distress with the following vital signs:• BP: 130/80 mmHg, CR: 115 bpm RR:35 T: 37.4

SKIN: Brown in color, moist, warm to touch, good skin turgor, no lesions, with healed wounds on the feet and petichiae on the extremities

HEENT: Icteric sclerae, pinkpalpebral conjunctiva, no nasal and aural discharge, no tonsillopharyngeal congestion, no cervical lymphadenopathy, no bruit, no anterior neck mass, no neck vein distension

PHYSICAL EXAMINATIONCHEST and LUNGS: Symmetrical chest expansion, no lagging, with retractions on the supraclavicular area, equal vocal and tactile fremitus, bibasal crackels

HEART: Adyanamic precordium, Tachycardic, PMI at 5th ICS LMCL, Normal rate , regular rhythm, no murmur

ABDOMEN: Flabby abdomen, normoactive bowel sound, tympanitic, soft, non tender to light and deep palpation

EXTREMITIES: Grossly normal extremities, no deformities, no external signs of cyanosis, with grade 1 pitting edema, with calf tenderness, full and equal pulses on the brachial, radial, and dorsalis pedis arteries

SALIENT FEATURES• 59 y/o male• 3 months PTA• (+) history of flood wading• 2 months PTA• (+) fever (undocumented)• Associated with:

– Myalgia• Not associated with:

– Difficulty of breathing– Rashes– Vomiting – Calf pain– Abdominal pain– Redness of the eye– Calf pain

• 1 week PTA– Diagnosed with UTII– Associated with urinary

symptoms• 4 days PTA

– Easy Fatigability– Decreased urine out put– Not associated with: – Fever, myalgia, bleeding,

rashes, yellowish skin or sclera, difficulty of breathing

• 1 day PTA – generalized body

weakness, • Few hour PTA

– difficulty of breathing– Not associated with

cough, back pain, chest pain, edema, dysphagia,

SALIENT FEATURES• Personal and Social

– Heavy alcohol beverage drinker

– Smoker with 5 pack yers

• Physical ExaminationPatient is, conscious, coherent, non ambulatory,in severe Cardio Repiratory Distress with the following vital signs:• BP: 130/80 mmHg, • CR: 115 bpm

• RR:35 • T: 37.4

- Petichiae on extremities

- Icteric sclera- Bi-basal crackles- Tachycardic- Grade 1 pitting

edema

ASSESSMENT

ACUTE KIDNEY INJURY SECONDARY TO LEPTOSPIROSIS MODERATE-

SEVERE

PLAN• FOR ADMISSION• IV PNSS 1L X200CC/hr• NPO temporary• Diagnostics:

• CBC WITH PC• Na, K, Cl• BUN, Crea• ABG• PT, PTT, INR• SGPT, SGOT• UA• Lepto MAT

• 12L ECG• CXR-PA

Therapeutics:– Cefrtiraxone 1mg TIV

now then OD– Furosenide 80gm TIV– Q8 with BP precaution– Omeprazole 40mg TIV

now then OD in AM– Vitamin K 30mg TIV now

then 10 mg TIV Q8

DISCUSSION

LEPTOSPIRA

• “Weil’s disease” • Severe

Leptospirosis• Characterized by:

– Fever– Jaundice– Acute Renal failure– Refractory shock– Pulmonary

haemorrhage

Epidemiological Factors

Occupation: (Dairy/Rice field/Sugar/Slaughter House workers Junkshop/Warehouse/Sewage/flood control workers,

Vet. Meds.)

Exposure to contaminated fresh pond/ flood waters Wading/ swimming/ Water related sports activities

PATHOPHYSIOLOGY

Pathogenesis: 3 mechanisms

• 1. Direct bacterial invasion

• 2. Non specific inflammation

• 3. Immunological reaction

Journal Inf. Dis.

Leptospira

Plasma pooling

Immunologic injury

Toxin production

Surface lipoprotein

OMP,LPS

Renal Ischemia

IN,ATN

Hepatic injury w/ subcelullar necrosis

Alveolar hemorrhage

Interstitial Myocarditis

Endothelial injury

vasculitis

VasculitisIP 2-28 days

Mandel, Principle of Inf Dse,5th edition Journal of Postgraduate Medicine, Vol. 51, No. 3, July-September, 2005

Dysregulation of Na-K ATPase

Pulmonary epithelial channel

LeptospirosisRenal involvement: 1. sub-clinical- mild proteinuria and few urinary

sedi- ments 2. Icteric Weil’s Syndrome (jaundice, renal dysfunction,

hemorrhagic diathesis) ARF (10% to > 60%) virulence, bacterial load, host immunity hyperbilirubinemia hypercatabolic with cholestasis

Leptospirosis

Renal involvement is common. 1. bacterial invasion 2. inflammatory process 3. hemodynamic alteration 4. direct toxicity of bacterial product Basic lesion is Interstitial Nephritis Glomerular changes are not remarkable Tubular Necrosis Acute Renal Failure primarily involves the PT

Leptospiral Nephropathy

Pathogenesis BACTERIAL INVASION/INFLAMMATION: Outer membrane protein-activates

monocytes- release of pro-inflammatory cytokines-

vasoactive substances and adhesion molecules Humoral response (Th1 and Th2 lymphocytes)deposition of IgM and C3 Cell mediated (cytokines and chemokines)


Hemodynamics: Pattern 2 ( seen in pulmonary hemorrhage ) cardiac index/SVR normal pulmonary vascular resistance increase

Pattern 3 ( seen in hyperbilirubinemia ) SVR slightly increase or normal CI, mean arterial pressure decrease pulm vascular resistance normal


HEMODYNAMIC CHANGES:Pattern 1 ( similar to sepsis ) SVR is decreased by nitric oxide CO, CI and blood volume increased Renal vasculature resistance

increased Renal blood flow and GFR decreased pulm vascular resistance normal + hypotension (60%)


DIRECT NEPHROTOXICITY Fluctuating renal tissue pH:

(virulence) ammonia recycling urinary acidification Bacterial cell wall (LPS) OMP –outer membrane proteins OmpL1, LipL41, LipL36


HYPOTENSION 1. renal ischemia 2. inflammatory processes

Renal Ischemia: dysregulation of lung salt and water channels downregulate pulmo epithelial Na

channel(ENaC), Na-K ATPase and aquaporin 5


Non-specific inflammatory factors:

hemolysis myonecrosis intravascular coagulation free radicals hyperbilirubinemia increased blood viscosity

Leptospirosis

Renal injury- is compounded by concomittant dehydration>>hypovolemia & hypotension, development of anuria>> poor prognostic sign.

In fatal cases- kidney are swollen & yellow w/ prominent cortical blood vessels.>>>focal areas of tubular necrosis.

Severe hemorrhagic Pneumonitis & Acute pulm distress syndrome- prominent manifestation of infection & occur in the absence of hepatic & renal failure.( CXR lower lobe evolve from small nodular densities Snow flakes like)

Leptospirosis

Human leptospirosis

Kidneys: swollen, bile stained interstitial edema, infiltration of

mononuclear cells and eosinophils ATN: Degeneration and necrosis of tubular epith cells

and disruption of basement membrane

Leptospirosis

Hemorrhagic Syndrome in Leptospirosis The basic pathomorphological substrate

endothelial damage leading to generalized vasculitis. studies have shown that capillary leakage and

hemorrhage result from the disruption of endothelial cell membranes of small vessels via the intercalation glycoprotein toxin w/c displaces the host long chain

fatty acids required to maintain vascular cell wall integrity.

Leptospirosis

and therefore: systemic vasculitides pulmonary hemorrhage ischemia to renal cortex destruction to hepatic architectiure

Leptospirosis

Chest X-Ray Findings:1. small, “snow-flakes like” nodular

density2. large confluent consolidation3. diffuse, ill-defined ground glass

appearance

DIAGNOSIS

Laboratory

Dark field microscopy – direct visualization of leptospires in blood & urine.

ELISA- 75% + to the patient on the day of admission to the hosp but not available commercially.

PCR(Polymerase Chain Reaction)only advantage is confirming the diagnosis during early acute phase of illness before the appearance of IgM ANTIBODIES.

In fulminating cases in which death occurs before seroconversion this test maybe of great value.

Histological Diagnosis relied on silver impregnation staining, but

immunohistochemical staining offer greater sensitivity & specificity.

Isolation and Identification leptospires can be isolated from blood, CSF,&

peritoneal dialysate fluid during first 10 days of illness. Specimen should be collected while the patient is febrile & before antibiotic therapy is initiated.

Urine can be cultured after the ist wk of illness. Culture are performed in Albumin polysorbate media –

incubated 30C x sev wks- slow growth.

Indirect Detection Method

MAT- ( Microscopic Agglutination Test) majority of leptospires cases

are diagnosed by Serology. Live antigen representing different serogroups of leptospires are reacted w/ serum sample & examined under Darkfield Microscopy fof Agglutination.

TREATMENT

TREATMENT

INDICATION DRUG DOSAGEChemo Doxycycline 200mg p.o. 1x/wkMild Lepto Doxycycline 100mg BID p.o. Ampicillin 500mgQID p.o. Amoxicillin 5oomg QID p.o.Mod-Severe PenG 1.5m IV QID Ceftriaxone 1g IV OD Ampi 0.5-1g IV QID

Treatment for Renal Involvement

• Acute Kidney injury– Plain NSS with potassium incoporation– Renal replacement theraphy for patients

in uremia, increasing creatinine of K levels, fluid overload, metabolic acidosis,

Treatment for Pulmonary Involvement

Methylprednisolone as Adjuvant in treatment of ARDS owing to Leptospirosis

methylprednisolone 40mg iv q 6 hr methylprednisolone 40mg iv q 8 hr methylprednisolone 40mg iv q 12hr x 2 oral prednisone 1 mg/kg taper in one

week

GUIDELINES

THANK YOU!!

Leptospirosis

Healthcare

Transcript of Leptospirosis