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COMMON TROPICAL INFECTIONS OF THE CVS 9

Dr. Debbi D. de la Fuente





TABLE OF CONTENTS MALARIA
1. Malaria (p. 1)
o Etiologic agents (p. 1) ETIOLOGIC AGENTS
o Life Cycle (p. 1) • Plasmodium falciparum – malignant tertian malaria
o Pathophysiology (p. 2) o More severe manifestations
o Morphology (p. 3) • P. vivax – benign tertian malaria
o Physiologic metabolic abnormalities (p. 4) • P. malariae – benign quartan malaria
o Complications (p. 4)
o Mechanism of host resistance (p. 4) Vector : Anopheles mosquito
2. Lymphatic Filariasis (p. 4)
o Etiologic agents (p. 4)
• Episodes of fever conicides with completion of the
o Vector (p. 4)
erythrocytic cycle
o Life Cycle (p. 4)
o Pathophysiology (p. 5) • Tertian Malaria – fever occurs every 3rd day (48
o Morphology (p. 5) hours)
o Spectrum of Disease (p. 5) • Quartan Malaria – fever every 4th day (72 hours)
o Complications (p. 5)
o Diagnosis (p. 5) LIFE CYCLE
o Brugia Malayi (p. 6)
3. Leptospirosis (p. 6) • 2 Stages of Malaria Life Cycle
• Etiologic agents (p. 6) o Exo-erythrocytic cycle (occurs in the liver)
• Transmission (p. 6) o Erythrocytic cycle (maturation of red cells)
• Pathophysiology (p. 6) § At end of Erythrocytic Cycle, red
• Spectrum of Disease (p. 6) cells rupture which coincides with
• Morphology (p. 6) the fever of patients with malaria.
• Physiologic consequences (p. 7)
4. Schistosomiasis (p. 7)
§ Etiologic agents (p. 7)
§ Intermediate host (p. 7)
§ Life Cycle (p. 7)
§ Pathophysiology (p. 8)
§ Complication (p. 8)
§ Morphology (p. 8)
5. Dengue (p. 8)
• Etiologic agents (p. 8)
• Vector (p. 8)
• Pathogenesis (p. 8)
• Pathophysiology (p. 8)
• Morphology (p. 9)
• Spectrum of Disease (p. 9)
• Laboratory Diagnosis (p. 9)
6. Chikungunya fever (p. 9)
• Etiologic agents (p. 9)
• Vector (p. 9)
• Pathogenesis (p. 9) Figure 1. Summary of Life cycle: Mosquito bite -> Sporozoites infect liver cells ->
mature to schizonts -> rupture to release merozoites -> merozoites infect RBC ->
• Symptoms (p. 9) ring stage trophozoites matureinto schizonts -> ruptures to release merozoites -
• Diagnosis (p. 9) > gametocyte. Blogg stage pararasites are responsible for clinical
manifestations. :

Topic (Lecturer):
Lecture Date:
3. Increased phagocytic activity in the liver and
PATHOPHYSIOLOGY spleen à hyperplasia of Kupffer cells, monocytes/

macrophages à hepatosplenomegaly
1. Parasitized RBC’s (Red cells that have been attacked by 4. Increased red cell destruction à anemia,
merozoites) will: hypotension, jaundice, hemosiderin deposition
5. P. falciparum stimulates production of cytokines
a. Adhere to each other (“cytoadherence” or
“rosetting”) & to (visceral) capillary endothelium P. falciparum Causes a More Severe Disease Because of the
(“intravascular sequestration”) producing fibrin thrombi à ff:
Ischemia/ microinfarcts due to formed microthrombi • It can infect RBCs of any age
• Causes infected RBCs to clump together and stick to
Brain – encephalopathy the endothelium
o PfEMP1 – facilitates sticking/rosetting/
Heart – CHF
cytoadherence to the endothelium
Lungs – pulmonary edema o When they stick to the endothelium, they
are sequestered in the small vessels
Other organs
resulting in decreased tissue perfusion
Lecture: This is especially true for P. falciparum. Intravascular • It causes GPI-linked proteins are released from the
sequestration mostly occurs in the deeper vital organs hence we infected red cells
only see the younger forms in the peripheral blood.
o Induces cytokine production by the host
cells (TNF, IFNy, IL-1)
b. adhere to normal red cells forming rosettes o Cytokines:
(aggregates) à easily sequestered or trapped in organs § Suppress RBC production
§ Induce fever
c. Be phagocytosed (with normal red cells) by fixed § Stimulate production of reactive
macrophages in the spleen & liver à increased red cell nitrogen species à tissue damage
destruction § Induce expression of PfEMP1
d. Be rigid with less deformability Plasmodium falciparum
• Sequestration of growing parasites in deep tissues
Lecture: Become rigid and less deformable may be due to changes in
phospholipid layer or red cell membrane, etc. à not able to pass where the environment favors their maturation
through the sinusoids à trapped à leads to their destruction • Ring forms are seen in peripheral blood

• They escape by the spleen and hence undergo
2. Ruptured RBC’s release: unbridled multiplication
a. Hemoglobin à hemoglobinuric nephrosis Pathologic Changes in Organs are Due to the Effects of:
*Excretion of Hb in the urine thus it turns
into a dark color • Adherence of red cells to each other and to vascular
endothelium à MICROVASCULAR OBSTRUTION
Lecture: Hemozoin – derived from the heme that results from the o Congestion & reduced blood flow
breakdown of Hb. Heme is considered toxic to the cell so parasites o Tissue hypoxia and microinfarcts
convert heme into a crystalized form (called Hemozoin). This
deposits in the organs such as spleen and liver making them have a • Destruction of both parasitized and normal cells
dark color o Rupture (INTRAVASCULAR HEMOLYSIS) –
breakdown of the red cells occurs within
the blood vessels
b. Malarial pigment (iron and protein; hemozoin) à § Anemia
slate gray or black spleen and liver
§ Jaundice
c. Parasites
§ Hypotension
d. Cells debris
§ Hemozoin deposition
e. Pyrogens à chills and fever
§ Hemoglobinuric nephrosis

§ Release of pyrogens

COMMON TROPICAL INFECTIONS OF THE CVS 2


Dr. Debbi D. de la Fuente
o Sequestration by fixed macrophages o Acute tubular necrosis & microinfarcts;
(EXTRAVASCULAR HEMOLYSIS) – acute renal failure (P. falciparum)
breakdown of red cells that have been o Hemoglobinuric Nephrosis (Blackwater
trapped in the liver and spleen Fever) due to acute hemolysis à dark urine
§ Increased phagocytic activity in o Quartan malaria: immune complex
liver and spleen mediated nephritic syndrome
§ Lymphoid and reticuloendothelial • Brain (Cerebral Malaria)
hyperplasia o Usually P. falciparum
§ Anemia o Edematous; surface is lead/ plum colored;
§ Hemosiderin deposition grayish cut surface appearance
o Small blood vessels congested with
EFFECTS OF MICROVASCULAR OBSTRUCTION
parasitized red cells
1. Congestion and reduced blood flow
o Larger vessels, parasites form a layer along
2. Tissue Hypocia and Microinfarcts
the endothelium (margination)
• Lungs – pulmonary edema, alveolar damage
o Ring Hemorrhages
• Kidneys –ARF
§ Petechial hemorrhages in the
• Brain – ring hemorrhages, neuronal
white matter
degeneration, Dürck’s granulomas
§ near occluded end arterioles
• GIT – mucosal necrosis and ulcerations
o Durck’s Granuloma
• Other organs - hemorrhages § small collections of microglial cells
MORPHOLOGY surrounding an area of
• Spleen demyelination at the site of
o Acute stage (primary attack): congested, hemorrhages
enlarged, soft (> 1000gms) o In severe hypoxia: neuronal degeneration
o Chronic: fibrotic & firm & focal ischemia
o Dark gray or black parenchyma due to • Heart
hemozoin deposition o Progressive anemia & circulatory stasis in
o Numerous macrophage with engulfed chronic malaria
parasites, red cells and debris o Petechial hemorrhages
• Liver o Occluded myocardial capillaries
o Enlarged and dark o Edema
o Kupffer cell hyperplasia; laden with malarial o Foci of degeneration
pigment, red cell and cell debris • GIT
o Malarial pigment in macrophages and o P. falciparum: mucosal edema, necrosis and
hepatocytes ulceration due to involvement of
• Bone Marrow splanchnic microcirculation
o Dyserythropoiesis
EFFECTS OF RED CELL SEQUESTRATION
o Erythrophagocytosis (INTRAVASCULAR HEMOLYSIS)
o Iron deposition
• Lungs • Anemia
o Acute pulmonary edema • Jaundice
§ due to capillary endothelial lesions • Hypotension -> Acute tubular injury and renal
& perivascular edema failure
o ARDS • Hemozoin deposition -> darkening of organs
o Capillaries and venules are packed with • Hemoglobinuric nephrosis (Blackwater fever)
inflammatory cells and parasitized red cells • Release of pyrogens -> chills and fever
o Bronchopneumonia, pneumonia, and
interstitial pneumonitis
• Kidney
o Acute malaria: transient glomerulonephritis

COMMON TROPICAL INFECTIONS OF THE CVS 3


Dr. Debbi D. de la Fuente
EFFECTS OF RED CELL RUPTURE ALSO: ­ cryoglobulins, autoAb, and HMW immune
(EXTRAVASCULAR HEMOLYSIS) complexes -> deposit in Kuppfer cells

• Increased phagocytic activity in the liver and spleen MECHANISM OF HOST RESISTANCE
• Lymphoid and reticulo-endothelial hyperplasia -> 1. Inherited alteration in red cells
hepatosplenomegaly • Absence of Duffy Antigen
• Anemia § Merozoite receptors are associaret with Duffy
• Hemosiderin deposition factors on red cells
PHYSIOLOGIC METABOLIC EFFECTS § If you do not have this antigen, you become
1. Blood volume becomes difficult to regulate resistant to malaria
• in the face of fever, moderate § West Africa: 90% lack Duffy factors
hyponatremia and increased capillary § Most blacks are insusceptible to P. vivax
permeability malaria
2. Anemia – due to repeated hemolysis o Sickle Hb Trait
1. Usually normocytic, hypochromic § confers resistance to P. falciparum
2. P. vivax – invades young cells o Parasitized red cells sickle much more
3. P. malariae – invades mature RBCs readily & hence are sequestered
4. P. falciparum – invades both à rapid o Hgb C
development of anemia in falciparum malaria o Resistant to osmotic lysis hence cannot
3. Thrombocytopenia burst & release merozoite
• due to sequestration of platelets in the o Modulates cell surface properties of
spleen infected red cell (decreased
aggregation)
4. Hypoglycemia – due to:
1. Glucose utilization by parasites 2. G6PD Deficiency
2. Inhibition of gluconeogenesis
3. Stimulation of ancreatic insulin secretion by • may limit Parasitemia
drugs like quinine
3. Repeated or Prolonged Exposure
COMPLICATIONS
• Generally, repeated infections are required to
1. Immune Complex Disorders
develop immunity
• Nephrotic syndrome
§ Immunity to one species does not
o Immune complex binds to basement
protect against other species
membrane of glomerular capillaries
§ Infants do not become infected
o Generation of C3a and C5a
during the first 3-4 months
o Accumulation of PMNs and macrophages

o Production of NO, ROS, and release of
LYMPHATIC FILARIASIS
enzymes
o Focal necrosis
o Glomerular sclerosis ETIOLOGIC AGENTS
• Tropical Splenomegaly Syndrome
o Hypersplenism • Wuchereria bancrofti
o High malarial Ab titers • Brugia malayi

o Elevated serum IgG & IgM
VECTOR
TROPICAL SPLENOMEGALY SYNDROME • Culex quinquefasciatus
Hyperactive malarial splenomegaly o in the tropics
In endemic areas (equatorial regions of Africa, Asia, • Others: Aedes, Anopheles, Mansonia
Middle East, South America)

Repeated exposures cause an exaggerated production if

IgM

Accompanied by lymphocytic inflitration in liver and
spleen
COMMON TROPICAL INFECTIONS OF THE CVS 4
Dr. Debbi D. de la Fuente
LIFE CYCLE o Subcutaneous fibrosis
o Epithelial hyperkeratosis

SPECTRUM OF DISEASE
• Asymptomatic Microfilaremia
o Microfilaria are present in the blood
without the patient experiencing symptoms
o Associated with filarial specific Th2 helper
cells that down-regulate Th1 helper cells
and
o inhibit granuloma formation
o Moderate enlargement of lymph nodes
o Numerous microfilaria in the blood
o Eventually adult worms die and microfilaria
disappear
o Usually seen in endemic areas where
children are exposed at an early age


Figure 2: Summary of Life Cycle of Filariasis: Mosquito bite → • Acute adenolymphangitis or recurrent
Filariform larva transferred to skin → penetrate skin → Lymphatic lymphadenitis
vessels & sinuses of lymph nodes → mature into adult worms that a. Sudden onset of high-grade fever, painful
mate → give rise to microfilaria → microfilaria penetrate walls of lymphadenitis, & lymphangitis
lymphatics → enter adjacent small blood vessels/ carried by lymphatic
b. 4-7 days (with 1-3 recurrences per year)
circulation to the blood stream
c. Funiculitis, epididymitis, orchitis, scrotal
PATHOPHYSIOLOGY edema (hydrocele)
d. Patients do not have microfilaremia
• Granulomatous reaction induced by adult worms in (microfilaria is damaged by the immune
lymphatics reaction)
o Mature worms in lymphatics induce
granulomatous reactions that become • Chronic lymphadenitis with elephantiasis
more pronounced when worms die → a. Develops after years of continuous filarial
occlusion/narrowing of lymphatics → infection
edema b. Damage to lymphatics is caused directly by
• Hypersensitivity to microfilaria adult parasites or by a TH1-mediated immune
o IgE-mediated (in tropical pulmonary response that stimulate granuloma formation
eosinophilia) around the parasites
c. Persistent chronic lymphadenitis & chronic
MORPHOLOGY lymphedema gives rise to fibroblastic
hyperplasia
1. Dilated Lymphatic Vessels in Adult Worms d. The high protein content of lymph stimulates
• Affects Lymphatics of Legs and Genitalia growth of dermal and collagenous connective
tissue →tough subcutaneous fibrosis;
• Thoracic duct/median abdominal lymph
epithelial hyperkeratosis; dilated dermal
vessels →scrotum and penis; external
lymphatics; lymphocytic infiltrates
genitalia in females
(elephantoid skin)
• Inguinal lymph nodes →extremities and
e. No microfilaria because the filaria disappear
external genitalia
after the worms die
• Dilated lymphatic vessels harbouring the

adult worms → causes lymphangitis
• Tropical pulmonary eosinophilia
(inflammation of the blood vessel)
o IgE mediated hypersensitivity reaction to
• Surrounded by mild inflammation
microfilaria: circulating IgE trigger mast cell
(sometimes none), eosinophilia with
degranulation
haemorrhage & fibrosis or granulomas
o Asthmatic episodes at night, with high
2. Lymphedema & Lymph Node Enlargement
peripheral eosinophilia and pulmonary
o Lymph nodes also harbour worms
infiltrates
3. Elephantoid Skin
COMMON TROPICAL INFECTIONS OF THE CVS 5
Dr. Debbi D. de la Fuente
o Eventually results in restrictive lung disease o Blood of patients may not contain
o Microfilariae do not appear in the blood microfilariae in some stages of the disease
because they are trapped in the lungs § It takes 6-12 months from the time of
infection until the worms mature
§ Microfilariae are not found in the early
ASYMPTOMATIC MICROFILAREMIA months of clinical inflammatory
• Moderate lymphadenopathy filariasis and in elephantiasis
• Numerous microfilaria in the blood • Detection of antigen & antibody
• In endemic areas where children are exposed at an o Ags of W. bancrofti – ELISA
early age immunochromatographic test

ACUTE ADENOLYMPHANGITIS OR RECURRENT Brugia Malayi
LYMPHADENITIS • Clinical manifestation are very similar to those of W.
• Sudden onset of high grade fever, painful Bancrofti
lymphadenitis and lymphangitis • More common occurrence of lymphangitis,
• Funiculitis, epidydimitis, orchitis, scrotal edema lymphadenopathy, and abscess-formation in the
• With fever, headache, vomiting, malaise inguinal lymph nodes
• 4-7 days; 1-3 recurrences per year • Elephantiasis is generally confined to the distal
• most patients do not have microfilaremia extremities
o involvement of the external genitalia is not
as common
CHRONIC LYMPHADENITIS WITH ELEPHANTIASIS
• recurrent lmyphangitis results in LEPTOSPIROSIS
o fibrosis • Weil’s Disease, Canicola fever, canefield fever,
o blockage of lymph flow nanukayami fever, 7-day fever
o chronic lymphedema • Invasion across epithelium followed by widespread
• Elephantiasis dissemination to various organs
• Rupture of dlated lymphatics • Direct tissue injury
o Kidney -> chyluria • Induction of mediators
o Tunica vaginalis -> hydrocoele or
chylocoele ETIOLOGIC AGENTS
o Peritoneum -> chylous ascited • Leptospira interrogans (spirochete)

TRANSMISSION
TROPICAL PULMONARY EOSINOPHILIA
• Via infected urine; contaminated water and soil
• IGE-mediated
• Pulmonary inflitrates PATHOPHYSIOLOGY
• Peripheral eosinophilia • Leptospira invades across the mucosa and non-
• Asthma-like attacks intact skin à widespread dissemination (Burrowing
• Microfilaria are trapped in the lungs but rarely action presumably accomplished by axial filaments
demonstrated & release of hyaluronidase)
• Eosinophilic abscess -> granuloma with FB-type
giant cells Mechanisms:
o Near pulmonary venules o Direct tissue injury
o Production of mediators: Endotoxin,hemolysin,
COMPLICATIONS lipase, cytokines
• Superimposed streptococcal infection (Acute
Dermatolymphangioadenitis) SPECTRUM OF DISEASE
• Cellulitis local pain & swelling, fever & chills 1. Anicteric (mild) Leptospirosis (90%)
• Septicemic Phase (4-7 days)
DIAGNOSIS o Absrupt onset of symptoms
• History of exposure to mosquitoes in endemic areas § Fever, shaking, chills, headache and
• Clinical manifestations myalgia, abdominal pain, conjunctival
• Demonstration of microfilariae suffusion
§ Less often: transient skin rash
COMMON TROPICAL INFECTIONS OF THE CVS 6
Dr. Debbi D. de la Fuente
o Septicemic pahse is followed by 2-3 days hemoptysis and pneumonia
of defervescence Kidney • Acute tubular necrosis à kidney
• Immune Phase (4-30 days; ave 14) failure
o Hallmarks: Aseptic Meningitis and Renal • Interstitial nephritis
Dysfunction • Petechial lesions on the surface
o Developmenet of antibodies (appearance Heart • Epicardial & endocardial petechiae
of IgM in serum) • myocardial edema
o Leptospire settle in glomeruli and are
• myocarditis
eliminated from all sites except the eyes
• coronary arteritis
and brain
o Fever and other constitutional symptoms
RES • Hyperplasia
may recur Muscle • Myositis; hemorrhage into muscle
o Leptospire from urine only beds = Rhabdomyolysis
2. Weil’s Disease (10%) – Icteric Leptospirosis Skin • Urticarial, petechial or
• Icteric leptospirosis desquamative lesions
• Usually casued by L. icterohaemorrhagiae CNS • Meningitis
• Persistent fever obscures the biphasic course Eyes • Acute Phase = vasodilation,
• Characterized by: subconjunctival hemorrhage, retinal
o Hepatic dysfunction (jaundice) vasculitis à suffesion (reddening of
o Renal failure (diffuse tubulointerstitial the eye surface)
nephritis, tubular necrosis) • Immune Phase = Iridocyclitis
o Hemorrhage (petechiae, purpura, GIT • Acalculous
conjunctival hemorrhage, GIT • Cholecystitis
hemorrhage) • Pancreatitis
o Multi-organ failure • GI bleeding
3. Sever Pulmonary Hemorrhagic Syndrome
• Hemoptysis, patchy lung inflitrates on x-ray,
respiratory failure (ARDS, total lung PHYSIOLOGIC CONSEQUENCES
consolidation) • Bleeding à anemia
• Renal failure
Note: Immune phase, detected via Urine while septicemic • Third spacing of fluids (due to increased
phase is detected via Blood permeability) à hypovolemia & vascular collapse
• ARDS
MORPHOLOGY
• Capillary Vasculitis (most consistent pathologic SCHISTOSOMIASIS
finding; Increased permeability) & leakage
o Endothelial edema, necrosis, and ETIOLOGIC AGENTS
lymphocytic inflitration • S. japonicum
• Leakage • S. mansoni
o Intraparenchymal bleeding • S. haematobium
o Petechiae
o Bleeding along serosa and mucosa INTERMEDIATE HOST
• Oncomelania (snail)
Organ/Organ Findings
System
Liver • Vascular congestion &
disorganization of the liver cell
plates
• Erythrophagocytosis by Kupffer cells
• Minimal necrosis of hepatocytes à
Jaundice; Hepatitis

Lungs • Alveolar capillary injury à edema;

bleeding (interstitial & intra-

alveolar hemorrhage) à cough,

COMMON TROPICAL INFECTIONS OF THE CVS 7
Dr. Debbi D. de la Fuente
LIFE CYCLE 3. Immunologic process resulting from cumulative
deposition of eggs
• Periportal fibrosis (Pipestem Fibrosis)
• Portal hypertension
o Congestive splenomegaly
o Varices
o Ascites
• Lungs
o Granulomatous pulmonary arteritis ->
poulmonary hypertension
• Heart – cor pulmonale

MORPHOLOGY
• Liver
o Portal fibrosis (pipestem fibrosis, Symmer’s
fibrosis)
Figure 3: Life cycle of Schistosomiasis • Spleen
o Congestive splenomegaly
Summary of Life Cycle
• Portal hypertension
1. Miracidium hatches out from excreted egg
2. Miracidia infect snails o Congestive splenomegaly
3. Cercariae is released from the infected snail o Esophageal varices
4. People are infected by contact with cercariae in water o Ascites
5. Cercariae enters skin and lose their tail to become o Hemorrhoids
schistosomulea • Lungs
6. Schistosomulea migrate through tissues, penetrate a o Granulomatous pulmonary arteritis with
blood vessel
intimal hyperplasia and obstruction ->
7. Brought to right heart and lungs
8. They squeeze through pulmonary capillaries into the pulmonary hypertension
systemic circulation portal vessels • Heart
9. Schistosomulea migrate in the hepatic portal venules o Cor pulmonale
and form pairs • Kidneys
10. Worm migrate against portal blood flow and deposit o Mesangioproliferative or membranous
egss into the mesenteric, vesical and pelvic venules
glomerulonephritis

PATHOPHYSIOLOGY (HOST RESPONSE) • Colon
• Much of the pathology is caused by host o Inflammatory patches or pseudopolyps
inflammatory reactions to the different stages of • Urinary bladder
the parasite o Hyperemia; vesicular or papular mucosal
1. Developmental stage (cercarial penetration to elevations
maturation of adult worms)
o Polyposis
• Transient itching and mild skin rash at area of
cercarial penetration o Calcific sandy patches
• Katayama fever o Ulcers
o Acute systemic illness 2 weeks after heavy o Contraction
exposure (fever, chills, weight loss, o Obstructive uropathy → UTI: due to
weakness, cough) inflammation and fibrosis of the ureteral
2. Period of active oviposition and egg excretion
walls
• Granulomas develop around the egg
• Egg secretes proteases and evoke local o Squamous metaplasia and dysplasia
inflammatory response o Squamous cell carcinoma (S. haematobium)
• Adult worms can cover themselves with host
protein hence immune system does not recognize
them

COMMON TROPICAL INFECTIONS OF THE CVS 8


Dr. Debbi D. de la Fuente
• S. mansoni – inferior mesenteric vein → distal colon o Spontaneous aggregation of platelets to
and liver infected endothelial cells → aggregation;
lysis and destruction
• S. haematobium – rectum, bladder, pelvic organs
o Anti-platelet antibodies
• S. japonicum – superior mesenteric vein → small
intestine, ascending colon, liver MORPHOLOGY
• Hemorrhages
COMPLICATION • Petechiae (DIC)
• Squamous cell carcinoma of the bladder
SPECTRUM OF DISEASE

1. Undifferentiated Fever
DENGUE • May be most common manifestation
2. Classic Dengue Fever (DF)
ETIOLOGIC AGENTS • Fever (5-7 days), headache, myalgia,
• Dengue virus bone/joints, rash (“break-bone fever”)
3. Dengue Hemorrhagic Fever (DHF)
VECTOR • Presence of plasma leakage differentiates this
• Aedes aegypti from DF
• Often occurs in second infections
PATHOGENESIS • Criteria:
• Person is infected with any dengue serotype → o Fever or recent history of acute fever
produces antibodies → antibodies form complexes o Hemorrhagic manifestations
with the virus → virus is neutralized o Low platelet count (100,000/cu mm or less)
• During subsequent infection by a new serotype, the o Objective evidence of leaky capillaries
pre-existing antibodies form complexes with the § Elevated hematocrit (20% or more
new virus but does not neutralize the new virus over baseline)
• The antibody antibody-virus complex enter a § Low albumin
greater proportion of monocytes than the virus § Pleural or other effusions
alone (Antibody-Dependent Enhancement) 4. Dengue Shock Syndrome (DSS)
• Infected monocytes release vasoactive mediators → • DHF + Circulatory Failure
increased vascular permeability and hemorrhagic
manifestations 4 Major Clinical Manifestations (in order of appearance and
frequency)
PATHOPHYSIOLOGY
1. Plasma Leakage 1. High-grade continuous fever (2-7 days)
• Most prominent feature 2. Hemorrhagic manifestations
• Pelural and peritoneal effusions • (+) tourniquet test
• Rising hematocrit o Test for capillary fragility
• Hypoproteinemia, hypoalbuminemia o DF: 10 or more petechiae per
2. Transient bone marrow suppression → decreased square inch
granulocytes o DHF: 20 or more petechiae per
3. Increased peripheral consumption and destruction square inch
of platelets (mediated by complement) → • Petechiae, epistaxis, GIT bleeding
thrombocytopenia 3. Hepatomegaly (days 3-4; in >90% of children)
4. Infiltration of vessel wall by lymphocytes and 4. Circulatory disturbances
macrophages → diapedesis of erythrocytes
5. Consumptive coagulopathy → shock LABORATORY DIAGNOSIS
• Demonstration of organism (blood, urine, CSF)
• Causes of Thrombocytopenia o Culture
o Complement activation o Dark field microscopy
o Virus induces bone marrow suppression o Immunofluorescence
o Virus binds to platelets & cause immune o Light Microscopy using special stains
mediated clearance of platelets § Silver stain
§ Warthin Starry stain

COMMON TROPICAL INFECTIONS OF THE CVS 9


Dr. Debbi D. de la Fuente
• Antibody detection (serologic exams)
o Radioimmunoassay (RIA)
o Enzyme Linked immunosorbent assay
(ELISA)
o Microscopic agglutination test (MAT)
• Molecular diagnosis (leptospiral DNA)- PCR


CHIKUNGUNYA FEVER

ETIOLOGIC AGENTS
• Alpha virus

VECTOR
• Aedes aegypti
• Aedes albopticus

PATHOGENESIS
• Pathogenic mechanism is similar to dengue
• Attacks human epithelial and endothelial cells,
fibroblast and monocyte-derived macrophages
• Self-limiting and lasts 2-3 days
• Recovery will confer life-long immunity
• Rarely fatal

SYMPTOMS
• High fever
• Joint pains (lower back, ankle, knees, wrist,
phalanges)
• Joint swelling
• Rash
• Headache, nausea, fatigue
• Muscle pain

DIAGNOSIS
• Rt-PCR
• Virus Isolation
• Serology (ELISA


REFERENCES
1. Lecture
2. Recordings
3. Online References

TRANSCRIBED BY:
o Group 23B
o Subtranshead: Mio Caguicla

COMMON TROPICAL INFECTIONS OF THE CVS 10


Dr. Debbi D. de la Fuente

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