HFRS vs Leptospirosis

7/29/2019 HFRS vs Leptospirosis

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Maisarah Repin Group 531-F

HFRS Leptospirosis

Acute zoonotic infection with a clear cyclic clinical syndrome with

febrile state, oligouric, polyuric & hemorrhagic syndrome

Definition Disease caused by variety of pathogenic spirochetes of the genus

Leptospira and is one of the most widespread zoonosis in the

world

Caused by viruses

Family : Bunyavirus

- Asian : Hantan viruscauses disease with prevalence of hemorrhagic syndrome

- Puumala virus (Puumala is a Finnish river) causespredominantly acute renal failure

Etiology Leptospira is highly coiled & mobile microorganism with a

hooked end. There are 79 serotypes that are pathologic to human.

They prefer alkaline, moist environment

Zoonosis

Main source = reservoirs/rodents latent CM of disease.

MOT : aerogenic (inspiration of dust with viruses), alimentary

(eating of food with viruses), close contact with viruses

Men > Women

Post infectious immunity is stable & life-long

Epidemiology Zoonosis

MOT : drinking/swimming in moist water can penetrate healthy

skin & mucous membrane. May enter through microwound of

skin

Primarily disease of animals

Men > infected

- Coal miners

- Harbours

Human-to-human spread is as rare as vertical transmission

Viruses fixed in regional LN and replicates during 1-7 weeks

Enter into blood stream, generalized viremia occurs

Massive viremia = Onset of Ds

Generalized vasculitis develop

Paresis of blood vessel

ITS develop

permeability of blood vessel & output of fluid into surrounding

tissues

Accelerate forming of BAS

coagulation of tissue proteins andforming of autoAg

Triggers into autoimmune

Damage BV and tissue

Maximal dose of viruses fix at kidney, its main target organ

damage

Oligoanuric period develop

Canals are damage

Polyuric dt canal function (disturbance of reabsorption). A lot of

extravasation in kidney may lead to kidney rupture

After Ab formation (end of 2nd week, >3-4 weeks) virus is

connected & eliminatedMain target damage

- BV : vasculitis & hemorrhagic fever

Pathogenesis After infection, microorganism fixate at regional LN and during

the next 3 weeks, multiplication takes place

Generalisation of process = generalized bacteremia

Vasculitis

Peculiarity : ability to penetrate Blood-Brain Barrier

In case of high dose of microbe, brain edema develop

Later, pathological process in cranial meningoencephalitis

Dissemination in 1st week

Toxic symptoms + Hemorrhagic syndrome

2nd

week : microorganism @ parenchymal organs- liver

-kidney

- spleen

Period of organ manifestation

- meningoencephalitis

- iridocyclitis

- hepatitis

- Renal Failure

- Hemorrhagic Syndrome

At end of 2nd week, antibodies form.

Short time improvement but in spite of blood Ab, tissue

immunity is absent.


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Clinical Course

first 5-6 days : Febrile

Next 3-4 days : Oligoanuric

Next 6-8 days : Polyuric

After : Reconvalescent

3rd & 4th week relapses

5th week strong immunity form, reconvalescence occurs

Ability to call non-sterile immunity

In accordance with pathology, the clinical periods are :

1) Initial febrile period (1 week)2) Organ manifestations3) Relapses (3-4th week)4) Reconvalescent ( 5th week)

Febrile

Abrupt onset

T up to high figures

Generalized toxicosis

Muscle and back pain

HA

Sx of HF hyperemia, enlargement of sclera vessels, hemorrhage at

sites of pressing, Red Cherry Sign (bleeding into sclera of eyes), +ve

tourniquette test, strong back pain (tenderness to percussion @

costovertebral angel reflect massive retroperitoneal)

Oligouric

In 5-6 days, T but patients condition becomes worse. Main Sx:

Abrupt of dieresis (dt no filtration), production of nitrogen

metabolism

Strong HA, BP (dt juxtaglomerular mechanism activation)

Renal eclampsia develop (high BP dt JG)

Renal encelopathy develops

- Loss of consciousness

- Apathy

- Tremor of lips, fingers

- Uremic colitis

Azotemic uremia - lvl of creatinine & urea in blood

Severe Hemorrhagic Syndrome

* bruises

* nose & teeth bleeding

* hematuria

Polyuric

In 3-4 days, dieresis restored & but its not reconvalescent. Its

Polyuric period.

Disturbance of tubular function (hypo and isosthenuria)

Clinical Manifestations Febrile

Looks like HFRS

Abrupt onset

T

Generalized toxicosis : HA, myalgia

Hemorrhagic syndrome

Loss of vision (dmg of retinal vessels)

Bruises

Symptom of red cherry

Difference : great risk of brain symptom development, strong

diffused muscle pain especially at calf muscle (dt lactate)

Organ Manifestation

Damage of liver

Jaundice

HSM

Change of liver enzymes

Damage of kidney (ARF same like HFRS)

Meningoencephalitis

- local Sx of damage of certain part of brain

- meningeal sx

Iridocyclitis

- refer to ophthalmologist

Relapse

At 3rd-4th week

Reconvalescence

At 5th week

Period of disappearance of CM & normalization of laboratory

values


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Reconvalescent

Reconvalescence lasts 1 year. In this period, maybe PN, kidney

rupture. Must be supervised by nephrologist

If patient presents with

- Fever suspect

- Hemorrhagic Syndrome HFRS

- Renal dysfunction

Must DDx with

Leptospirosis

Rickettsia

Flu

Sepsis

Method of specific Ix

- luminescent reaction of Ab reaction

- only after 2nd week!!

Febrile Oligouric PolyuricGBT Leucopenia

Lymphocytosis

Monocytosis

ESR is normal

Leucocytosis

ESR

Anemia

TCP

Neurophilosis

w/o changes

Urine

analysis

w/o change density

High,

transient

proteinuria

Hematuria

()

Casturia

Epithelial

cells

Hypoisosthenuria

Biochemistry

creatinine

K

BUN

Oligoanuric : control these factors everyday to see dynamics and

indications to hemodialysis

Investigations &

Diagnosis

Leptospira x grow into media

Serologic

Passive hemagglutination

Pair serum

1st : 2nd week or less 2nd : in 7-10 days

titre confirms the diagnosis

Sometimes material from patient maybe diagnosed using dark-

field microscopy (x stain with aniline)

They are transparent & motile


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Febrile

Infective Toxic Shock

Oligoanuric

Kidney rupture ( even during Pasternatsky sign elicitation!)

- Unilateral back pain

- BP

- Anemia- Abdominal palpation infiltrate hematoma

Rx : Surgery

Renal Eclampsia

- repeated alteration of tonic-clonic cramps dt BP

Azotemic Uremia

- Renal encephalopathy

Complications At 4th-5th week

- Infectious Allergic Complication!

* GN

* Pancreatitis

* Myocarditis

During late reconvalescent, of hearing & vision may develop

Post-leptospirosis Cx

- Leptospira Ictera-Hemorrhagia of Polyorgan Failure

- Will-Vaselev disease (?)

Depends on stage

Febrile

Traditional solutions (5% glucose, 0.9% NaCl)

Restore BV wall (Vit C, Ca)

Steroids microcirculation (rheopolyglucine, trental)

Analgesics

Oligoanuric

Diuretics + 1L = volume of detox infusion

Diuretics :

80mg Furosemide (lasix). If dieresis x , then diuretics are CI!!

Non-efficacy :

- 10% 10ml CaCl2

- 2.4% 10ml euphylline

- 0.25% Novocain (100-150ml)

IV drops

At end of injection, add 10-20% 10ml Glucose, 6-8 Units of insulin

to transform extracellular K+ into intracellular space (if

hyperpotassemia)

Meteorism

vomiting

arrhythmia

bradycardia

Inject 10% NaCl!

Treatment Early antibiotic therapy

Penicillin

6-12 million Units/day IM q4-6hours

To prevent relapses, at 3-7 days add tetracycline 0.3mg qid for 5days.

Other methods are the same as HFRS!

After reconvalescent, must supervise for 6 months to prevent

late complications!


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Hemorrhagic Syndrome

Vit C

Na ethamzilate

Fresh frozen plasma (FFP)

If x efficacy add Dopamine (very slow injection to enlarge renal

vessels)

If x efficacy during 1 day, estimate indication for hemodialysis.

Indications:- Oliguria >4days

- non-protein nitrogen > 60

- BU >20

- K+ > 7mmol

Polyuric

Restore salt maintenance

Inject poluion salt solution

Rule of discharge?

Mild

2 weeksModerate 3 weeks

Severe 4 weeks

Supervise for 1 year!

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HFRS vs Leptospirosis