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Unformatted text preview: TROPICAL MEDICINE FOR THE
DISEASE,AMOEBIASIS,LEPTOSPIROSIS) DR.AMIT RAODEO MALARIA 1 INTRODUCTION
Malaria remains a major public health problem in endemic
Responsible for 1.5 to 2.7 million deaths each year worldwide.
Tropical African countries are estimated to contribute >90% of
the total malaria incidence and great majority of malarial
Respiratory tract involvement ranging from upper respiratory
symptoms to ARDS is seen in 3-10% cases.
3Incidence of pulmonary edema was around 1per 1000 cases in
a large study from vietnam.
vietnam. SEVERE MALARIA
Definition:Presence of P.falciparum asexual parasitaemia and no other
obvious cause of their symptoms,the presence of one or more of the
following clinical/laboratory features is classified as severe malaria
hyperparasitaemia 2 COMPARISON BETWEEN
LEPTOSPIROSIS,MALARIA AND DENGUE
difference Leptospirosis Malaria dengue Splenomegaly + ++ + or - Subconjunctival
hemorrhage Classically present Can be present
Rare Can be present Myalgia Classically present Usually
present Can be present Hemoptysis Common Uncommon Uncommon Encephalopathy Uncommon Common Uncommon Abdominal pain Common Uncommon Uncommon Arthralgia Less common Uncommon common COMPARISON BETWEEN LEPTOSPIROSIS,MALARIA AND DENGUE
Lab difference Leptospirosis Malaria Dengue Hemoglobin Normal unless bleeding Anemia Elevated/normal unless
bleeding TLC Leucocytosis Usually
normal,leucocytosis can be
Increased TLC bad
prognostic sign Normal/leucopenia Potassium levels Hypokalemia common
/hypokalemia Normal/raised/reduced DIC Uncommon Common Common P.S Left shift Malarial parasite Atypical lymphocyte Hypoglycemia Uncommon Common Uncommon Pulmonary involvement Pulmonary hemorrhage
Diffuse nodular shadows
due to parasite Less common ALI/ARDS ABG Normal anion gap,acidosis
more common High anion gap metabolic
acidosis(lactic) Lactic acidosis less common Ascites / bilateral pleural
effusion Absent Absent Present Myocarditis Common Less common Less common 3 HOW COMMON IS MALARIA AS CAUSE OF ARDS? PATHOGENESIS OF ALI/ARDS IN MALARIA 4 PATHOGENESIS OF ARDS AND PULMONARY EDEMA
IN MALARIA DIFFERENTIAL DIAGNOSIS OF HYPOXEMIA IN
Gram negative bacteremia
Sequestration of parasitised RBCs in pulmonary
vasculature 5 BACTERIAL SUPERINFECTION IN MALARIA
Both community acquired as well as nosocomial infections
2)Impaired splanchnic perfusion-translocation of gut
Most common infection is aspiration pneumonia.
Recommendation:-Empirical antibiotics in severely ill
Recommendation:patients without delay. COMMUNITY ACQUIRED BACTERIAL INFECTIONS IN
MALARIA(n=93) LESS SEVERE
MALARIA Number of episodes 13(14%) 6(6%) Number of patients 13(14%) 6(6%) Site of infection 17 6 Pneumonia 6 1 Bacteremia 5 1 Urinary tract infection 3 1 Miscellaneous 3 3 6 LAB DIAGNOSIS OF MALARIA
METHOD ADVANTAGE 1) Thick blood film • DISADVANTAGE Sensitive(0.001% parasitemia)
•Inexpensive. Requires experience.
Underestimates true count. •
•Provides prognostic information
in severe malaria. •Insensitive (>0.05%
•Uneven distribution of P.vivax.
Sensitivity similar to or slightly
less than thick film (>0.001%
parasitemia). Detects only P.falci.
Remains +ve after weeks of
•Does not give quantitative
analysis. 4) Plasmodium LDH dipstick or
card test Rapid
Sensitivity similar to
•Less sensitive diagnosis for
P.vivax,malarie and ovale.
ovale. •Slightly more difficult than
•Miss low levels of parasitemia
with other malarias.
•Does not provide quantitative
analysis. 5)Membrane concentration
methods with acridine orange
staining •Sensitivity similar or superior to
that of thick films (~ 0.001%
•Ideal for processing large no. of
samples rapidly. Does not specify or quantitate.
microscopy. 2)Thin blood film •
• 3)PFHRP2 dipstick or card test •
• PROGNOSTIC MARKERS IN MALARIA
(n=10) P VALUE Unrousable
coma,n(%) 25(30) 9(90) <0.001 Severe anaemia,n(%) 7(8)
anaemia,n(%) 1(10) 1 Renal failure,n(%)
failure,n(%) 40(48) 7(70) 0.3 Pulmonary
edema,n(%) 5(6) 5(50) <0.001 Hypoglycemia,n(%)
Hypoglycemia,n(%) 3(4) 0 1 Shock,n(%)
Shock,n(%) 12(15) 8(80) <0.001 Bleeding/DIC,n(%)
Bleeding/DIC,n(%) 19(23) 3(30) 0.7 Seizures,n(%)
Seizures,n(%) 2(2) 0 1 Acidosis,n(%)
Acidosis,n(%) 11(13) 8(80) <0.001 Coma and
acidosis,n(%) 2(2) 8(80) <0.001 Coma and
shock,n(%) 3(4) 8(80) <0.001 Parasitemia of more
than 5%,n(%) 32/79(41) 7/9(78) 0.07 7 TREATMENT OF SEVERE FALCIPARUM MALARIA Trial No. of
(SEAQUAMAT) 1461 Wellcome Trust
Clinical Research 560 Unit Faculty of Tropical
University 131 Faculty of Tropical
University 102 Drugs Results Reference Artes(730)
mortality Lancet 2005; 366:
clearance N Engl J Med. 1996
mortality Clin Infect Dis. 2003
mortality Trans R Soc Trop
Med Hyg. 1995 NovHyg.
Dec;89(6):668- CURRENT RECOMMENDATION
Artimisinin derivatives like artisunate , artimether are drug of
choice for severe malaria.
Artisunate has the advantage of being water soluble and can be
given I.V. 8 CURRENT RECOMMENDATION FOR
EXCHANGE BLOOD TRANSFUSION
Currently there are no randomized control trials to show any
benefits of exchange blood transfusion over conventional
Procedure is hazardous and availability of blood is a limiting
Currently WHO does not recommend exchange blood
transfusion in the management of severe malaria. OTHER ADJUVANT THERAPY
No survival benefit
Pentoxyfylline - No established role
Anti 9 ROLE OF aPC IN MALARIA/LEPTOSPIROSIS
scenario Inference Reference Drotrecogin alfa
(activated) in severe
falciparum malaria severe falciparum
MODS aPC for 96 hrs f/b
improvement Anaesthesia, 2006,
61, pages 899–902
899– Case series of 10
tropical infections Includes 4 cases of
falciparum and I
leptospirosis 1 out 4 died Intensive care Med
1282 LEPTOSPIROSIS 10 INTRODUCTION
Transmitted by contact with infected urine and rarely
blood of infected rodent.
Penetration recurs through intact mucous membrane
or abraded skin. PATHOGENESIS Septicemic phase – vascular injury
Immune phase – immune complex deposition
Immune 11 PATHOGENESIS OF LUNG INJURY
In contrast to liver and kidney, isolation of leptospires is
uncommon from lung tissue.
Antigenic debris is also less common in lungs.
Widespread but subtle inflammatory process.
Presence of antibody along the septal wall in infected guinea
pigs may suggest an autoimmune response similar to
Goodpastures disease (Abs to type IV collagen).But renal
tissue did not reveal glomerulonephritis characteristic of
The exact mechanism is largely unknown.
The CLASSICAL FEATURES OF LEPTOSPIROSIS
Biphasic illness -1)Septicemic phase
2)Brief afebrile period
(liver and kidney)
Diagnosis in early phase is commonly missed.
Hence Faine proposed a clinical scoring system which has
good sensitivity (81.8%) and specicity(72.9%).
Usually helpful in excluding diagnosis because of high
negative predictive value.
J Postgraduate Med.2005 Sept.51(3),169
Post 12 LUNG INVOLVEMENT
Ist publication of lung involvement in leptospirosis is
attributable to Moeschlin in 1943.
Varies between 20%-70% in all cases in various studies.
20%Pulmonary examination ranges from normal to extensive
alveolar hemorrhage and respiratory failure.
Patients with severe alveolar hemorrhage can die within 24
BAL examination in patients with leptospirosis by D u couedic
and colleagues found that alveolar hemmorrhage was present
in all patients with sign /symptom of respiratory involvement
and 7/10 patients in asymptomatic patients.
Trop.1992,25:21- 13 LUNG INVOLVEMENT (CONTD)
There is absence of significant inflammation in areas of
Usually associated with hepato-renal involvement but can
hepatooccur in the absence of these. J.Infect.Disease.1998;178;1457-63
J.Infect.Disease.1998;178;1457- LAB DIAGNOSIS OF LEPTOSPIROSIS
TEST ADVANTAGE DISADVANTAGE DGM Convenient Lacks sensitivity and
staining Can be done on blood,
urine or rarely CSF. 10,000 leptospira/ml for
visualization is necessary. Immunoperoxidase
staining Can be done on blood,
urine or rarely CSF. 10,000 leptospira/ml for
visualization is necessary. A)MICROSCOPY 14 LAB DIAGNOSIS OF LEPTOSPIROSIS
TEST ADVANTAGE DISADVANTAGE B) SEROLOGY
Requires maintaining strains
Detects group specific Abs. for preparation of Ag. IgM ELISA Most widely used
( sensitivity 100% and
specificity 93%) IgG ELISA High rate of false positive. Indirect Fluorescent Rapidity
agglutination High sensitivity and
specificity CIEP LAB DIAGNOSIS OF LEPTOSPIROSIS
TEST ADVANTAGE DISADVANTAGE C) Culture Gives confirmed diagnosis Low sensitivity
Requires atleast 1 month before
can be declared negative D) Molecular diagnosis
2)In situ hybridization
3)PCR Useful for DNA detection in
serum and urine.
Useful when other tests fail to
Used for post mortem
diagnosis. Inability to identify serovar.
Cost and availability. 15 PROGNOSTIC MARKERS
Multivariate analysis revealed three variables associated
disturbance 6 (CI 0.9-38.5)
0.9- 0.005 Serum
ol/l 0.02 Serum potassium>4 19.9 (1.2-342)
(1.2- 0.009 TREATMENT OF LEPTOSPIROSIS
Ceftriaxone was found effective in severe
leptospirosis in a study by Raptis et al .
23 patients were given ceftriaxone out of which 21
survived.No significant ADR noted. Int J Antimicrobial Agent 2006 Sept,28(3);259-61
Sept,28(3);259- 16 TREATMENT OF LEPTOSPIROSIS
A prospective,open label, randomized trial in
Thialand was conducted in 2000-2001,where they
compared ceftriaxone(1 gm/day for 7 days) with
sodium penicillin G (1.5 MU 6 hrly for 7 days).
Both were found equally effective with median
duration of fever was 3 days and equal number of
deaths (5) were found in each group. ROLE OF STEROIDS IN LEPTOSPIROSIS 17 AMOEBIASIS INTRODUCTION
Protozoan infection caused by Entamoeba histolytica.
Third most common cause of death from parasitic diseases
after malaria and schistosomiasis worldwide.
Extraintestinal manifestations are the most comon cause of
death. 18 EXTRAINTESTINAL SITES INVOLVED
5) Amoebic liver abscess-most common.
abscessPleuro-pulmonary – second most common.
Genitourinary tract. RISK FACTORS FOR AMOEBIASIS 5) Lower socio-economic class
Lack of safe drinking water
Travellers 6) Prisoners 1)
4) 19 RISK FACTORS FOR PULMONARY
ASD with left to right shunt MODES OF PULMONARY INVOLVEMENT
Primary - Very rare
- Inhalation of dust containing cysts.
- Aspiration of cysts or triphozoites of
Secondary- Hematogenous spread from colon.
Tertiary - Most common. Extension of amoebic liver abscess
Tertiary 20 ROUTES OF INVOLVEMENT
Routes of involvement
1) Abcess extending from
3) Empyema extending from
4) Hematogenous spread
without liver involvement
5) Hematogenous lung abcess
and independent liver abcess Percent
10.4 TYPES OF LUNG INVOLVEMENT
Types of lung involvement
1) Heptobronchial fistula
2) Pleural effusion and
3) Lung abscess
4) Consolidation Percent
10 21 CLINICAL FEATURES
Fever of weeks duration and right upper abdominal and right
pleuritic type of chest pain.
Dramatic presentation of severe pain,respiratory distress and
Hepatomegaly in 50% cases.
Hemoptysis is common followed by expectoration of
ancchovy sauce like pus.
Bile in sputum is important clue toward hepatic origin.
When to suspect amoebiasisWhen
4)Basal pulmonary involvement in patient from endemic area >3
years age. 22 DIAGNOSIS 1) 2)
5) Lateral radiograph: Lateral
Upward hump like prominance which can be anterior,
middle or posterior.Anterior hump is more common.
Consolidation which may have cavitation.
HydropneumothoraxCavity with air fluid level in case of bronchial
Stool examionation :Limited value.
Only positive in 15-33% cases of extraintestinal amoebiasis.
Pathogenic and nonpathogenic amoeba can be differentiated
by zymodeme analysis,ELISA,RFLP.
Sputum examination ::Usually sterile and paucicellular unless superinfected.
superinfected. 23 ROLE OF ULTRASONOGRAPHY
Monitoring response to therapy.
To detect small pleural effusion.
To look for subpulmonic collection.
To differentiate from bacterial empyemas – loculations and
septations are rare in amoebic empyemas.
empyemas. WHAT IS ROLE OF CT SCAN?
Can detect intrapleural fluid anywhere in the thorax example
beneath scapula or within fissure which is usually missed by
Guide interventional procedure.
To differentiate empyema with bronchopleural fistula from
lung abscess. 24 IMMUNOLOGICAL TESTS IN AMOEBIASIS
2)ELISA for IgG and IgM , IgM is more specific 3) IFAT
B)NewerB)Newer1) Gal or GalNAC inhibitable - Potential role in extraintestinal
adherence lectin IgM
2) Gal-GalNAC Ag by ELISA- >90% sensitivity before
3) E.histolytica Ag detection kit- useful for sputum and pleural
4) DNA by PCR- most sensitive method of detection of pleuropulmonary
amoebiasis. DIFFERENTIAL DIAGNOSIS OF AMOEBIASIS
Presence of palpable liver can be mistaken as secondary.
Anterior basal segment of right lower lobe involvement is
characteristic of amoebic origin. 25 TREATMENT OF AMOEBIASIS
Oral or parentral metronidazole 800 mg (35-50 mg/kg/day)
(35three times daily for 5-10 days is the treatment of choice.
5Chloroquin and emetine are other alternatives but should be
avoided because of potential cardiovascular side effects. PULMONARY HYDATID 26 INTRODUCTION Hydatidosis is one of the most geographically
widespread zoonoses in the world.
Four species of Echinococcus are recognised.
Four EPIDEMIOLOGY OF HYDATID DISEASE
Species Geographical Definitive Intermediate Transmission
us Dogs Sheeps Feco-oral route
Feco- Rodents Ingestion Europe,Africa,South
New Zealand E.multiloc Arctic,Asia,Wester Foxes,
n central europe
E.Vogeli South America --- --- E.oligarthia South America --- --- 27 LUNG INVOVLEMENT IN HYDATID
Through transdiaphragmatic thoracic involvement- most
Lymphatic LUNG INVOLVEMENT IN HYDATID
Sometimes lesions develop in area of lung remote from
3)Rupture of liver abscess into inferior vena cava and
thromboembolic disease which may progress to pulmonary
hypertension and cor pulmonale.
pulmonale. 28 PLEURO-PULMONARY MANIFESTATIONS OF
HYDATID HYDATID CYST RUPTURE PLEURAL SPACE BRONCHUS ASYMPTOMATIC PRESSURE EFFECT COUGH DYSPNOEA PNUEMOTHORAX PERSISTENT PNUEMONIA PLEURAL EFFUSION RECURRENT HEMOPTYSIS EMPYEMA CHEST PAIN VOMIT LIKE CYSTIC FLUID ALLERGIC OR ANAPHYLACTIC REACTION DIAGNOSIS OF HYDATID DISEASE
1) Specific serum antibodies.
2) Chest X-ray –
XSolitary lesions- 60% cases.
Solitary lesionsMultiple –unilateral/bilateral lesions in 25-50%.
25Ruptured cyst-Consolidation surrounding area.
Ruptured cystIt communicates with bronchus-air fluid level.
bronchusMiniscus sign or crescent sign.
Cumbo’s sign (onion peel sign).
Water lily sign.
Mass within a cavity.
Inverse crescent sign.
Inverse 29 TREATMENT OF PULMONARY HYDATID
Surgery is the mainstay of the therapy – as complete
elimination of parasite can only lead to cure.
The principle is to preserve as much lung tissue as possible.
Akin et al observed that radical resection is too aggressive and
often not necessary.
Paraenchyma around a hydatid cyst is often affected by lesion
and may show chronic
congestion,hemorrhage,bronchopneumonia or interstitial
These changes often resolve after surgery, hence parenchymal
resection is rarely indicated. TREATMENT OF PULMONARY HYDATID (CONTD)
Conservative surgery are preferred.
4)Cystectomy with cappitonage.
Spillage of daughter cyst is to be avoided.
Recurrence can occur but fresh infection is also reported in
person living in endemic area.
Bilateral pulmonary hydatid :One stage/two stage surgery.
Larger cyst/ruptured cyst area treated first.
Larger 30 RECENT ADVANCES N THE TREATMENT OF
Thoracophrenotomy is less invasive & preferred method of
surgery in cases of combined lung & liver hydatid
Br.J.surg.2005;92(6);729- Recent reports have described VATS in pulmonary hydatid.
Recent CAN J SURG.2004;47,380-381
SURG.2004;47,380- TREATMENT OF PULMONARY HYDATID (CONTD)
Advocated by few authors.
68-70% of patients with pulmonary hydatid show some degree
25-34% cure rates have been documented.
25Considering high risk of complications, hydatidosis patients
should be followed closely.
PARASITOL.INT.2005;54;135- 31 DRAWBACKS OF MEDICAL THERAPY
Poor compliance and ADR due to long course of treatment.
Poor follow up – most patients are from rural areas.
Poor cure rates.
High risk of complications.
Lung hydatids produce more complications than liver,hence all
patients of pulmonary hydatid irrespective of size or
presence/absence of complications are to be surgically treated.
Medical therapy should be used to prevent recurrence.
Recommended regimen – mebendazole 1 month preoperative
& 3 interrupted courses postoperatively 32 TROPICAL PULMONARY
EOSINOPHILIA (FILARIASIS IN
One of the many syndromes with pulmonary infiltrates and
peripheral blood eosinophilia.
Originally described in India in 1940.
ILD thought to be due to immunological hyperresponsiveness
to human lymphatic dwelling filarial parasites-W.bancrofti and
B.malayi. 33 DIAGNOSTIC CRITERIA FOR TPE
Cough worse at night.
count >3300/cube mm.
Clinical Residence in filarial endemic areas.
Eosinophil and hematological response to DEC.
Filarial antibody test has little value. RESP. MED. 1999;93;655-659
Out of 90 million people infected worldwide,<1%
manifest symptoms of TPE.
Exact reason is not known.
Intense inflammation of lung parenchyma to trapped
microfilaria which are released into circulation by
adult worms residing in lymphatic system.
Microfilaria are always absent in peripheral blood
Sometimes detected in lung biopsy specimens.
Sometimes 34 PATHOGENESIS (CONTD…)
BAL of affected individuals reveal that polyclonal IgE and
filarial specific IgM,IgG and IgE accumulate in the lung.
Profound dysregulation in otherwise tightly regulated IgE Ab
Limited evidence to suggest underlying genetic basis.
Usually complete resolution after therapy with DEC but in
some cases some degree of irreversible interstitial fibrosis
Pathogenesis in some aspects analogues to atopic asthma
- obstructive ventilatory picture.
- partial reversibility with beta2 agonists.
- high levels of serum IgE.
IgE. 35 ...
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This note was uploaded on 12/03/2011 for the course MEDICINE 350 taught by Professor Dr.aslam during the Winter '07 term at Medical College.
- Winter '07