Ascaris lumbricoides

Ascaris lumbricoides is an intestinal round worm. It is the largest intestinal nematode to infect Human. The
adult worm lives in small intestine and grow to a length of more than 30 cm. Human is only the natural host
and reservoir of infection.

The round worm infection occurs worldwide. The number of infected persons is estimated to be more than
2 billion. The main epidemic region with prevalence rate of approx. 10-90% includes countries on South
east Asia, Africa and latin America.

Morphology:

Adult:

The round worm resembles to earthworm. It is elongated tapering to both end, anterior being thinner than
posterior. Freshly excreted worm is yellowish pink in color, which gradually changes to white.

The worm is sexually diamorphic.

 Adult male: 15-30 cm in length, 3-4 mm in diameter, tail curved
 Adult female; 20-40 cm length, 2-6mm diameter, tail straight

Egg:

Ascaris egg is round or oval, 60*40 µm size, thick brown shell and have rough surface. It is the infective
form of parasite.

 i) Un fertilized egg; large, more elongated (38-55*78-105) µm

 ii) fertilized egg; ovoid (35-50*50-70)µm, golden brown color

Life cycle:

The life cycle of Ascaris completes in single host. Human.

 Adult worm lives in small intestine

 Stages in life cycle:

Stage I: Eggs in faeces

 Sexually mature female produces as many as 200,000 eggs per day, which are shed along with faeces
in unembryonated form. They are non infective.

Stage II: Development in soil

 Embryonation occurs in soil as optimum temperature of 20-25C with sufficient moisture and O2
 Infective larva develops within egg in about 3-6 weeks.

Stage III: Human infection and liberation of larvae

 Human get infection with ingestion of embryonated egg contaminated food and water
 Within embryonated state inside egg, first stage larvae develops into second stage larvae. This second
stage larvae is known as Rhabtitiform larvae
 Second stage larve is stimulated to hatch out by the presence of alkaline pH in small intestine and
solubilization of its outer layer by bile.

Stage IV: migration of larvae through lungs

 Hatched out larvae penetrates the intestinal wall and carried to liver through portal circulation
 It then travels via blood to heart and to lungs by pulmonary circulation within 4-7 days of infection.
 The larvae in lungs molds twice, enlarge and breaks into alveoli.

Stage V: Re-entry to stomach and small intestine

  From alveoli, the Larvae then pass up through bronchi and into trachea and then swallowed.
 The larvae passes down the oesophagus to the stomach and reached into small intestine once again.
 Small intestine is the normal habitat of Ascaris and it colonises here.
 Within intestine parasite molds twice and mature into adult worm.
 Sexual maturation occurs with 6-10 weeks and the mature female discharges its eggs in intestinal
lumen and excreted along with faeces, continuing the life cycle.
 The life span of parasite is 12-18 months

Pathogenesis:

1. Mode of transmission:

 faeco-oral route, by contaminated vegetables or water.

2. Pathogenesis:

Infection of A. lumbricoides in man is known as Ascariasis. There are two phase in ascariasis.

Phase I: migrating larvae

 The migrating larvae causes pathological lesions. The severity of lesions depends upon the sensitivity
of host, nutritional status of host and number of migrating larvae.
 During migration and molding through lungs, larvae may causes pneumonia with low grade fever,
cough and other allergic symptoms.

Phase II: Adult worm

 Few worm in intestine produce no major symptoms and but some time give abdominal pain
especially in children.
 The adult worm produce trauma in host tissue and the wandering adults may block the appendical
lumen or common bile duct and even small intestine.
 Large number of adult worms affects the nutritional status of host by robbing the nutrition leading to
malnutrition and growth retardation in children.
 The metabolites of living or dead worm are toxic and immunogenic.
 lumbricoides also produces various allergic toxin, which manifests fever, conjunctivitis and irritation.

Clinical manifestation:

Most of the Ascaris infection is asymptomatic.

1. Symptomatic ascariasis; two types

2. Intestinal Ascariasis
3. Pulmonary Ascariasis

1. Intestinal ascariasis;

 Nausea
 Vomiting
 Colicky abdominal pain
  Abdominal distention
 Weight loss and diarrhea
 Malbasorption of nutrition
 Growth retardation
 Heavy worm in children leads to intussusception and total obstruction
 Complications: Appendicitis, Biliary colic and perforation of bile duct, Hepatomegaly

2. Pulmonary ascariasis;

 Transient eosinophilic pneumonitis (loeffler’s disease); elevated IgE

 Bronchospasm
 Dyspnea and wheezing
 Fever
 Non-productive cough and chest pain

Lab diagnosis:

1. Specimen: stool, sputum

2. Microscopy: examination of stool by saline emulsion or concentration by floatation methods
employed to unembryonated egg
3. X-ray
4. Serodiagnosis: Indirect haemagglutination test, Immuno-fluorescence assay
5. Ultrasonography and CT scan
6. Other test: blood count shown peripheral eosinophilia

Treatment and prophylaxis:

 Mebendazole: drug of choice, (100mg twice a day for 3 days)

 Albendazole: 500mg single dose
 Pyrantel pamoate: single dose of 1omg/kg weight
 Piperazine citrate
 Entamoeba histolytica
Entamoeba histolytica is a common protozoan parasite found in the large intestine of human. The parasite is
responsible for amoebiasis and liver absceses. It is the third leading parasite cause of death in the developing
countries.

Morphology:

Parasite occurs in three stages; trophozoite, precyst and cyst

1. Trophozoite:

 It is the growing and feeding stage of parasite

 Sape; not fixed because of constantly changing position
 Size: ranging from 18-40 µm; average being 20-30 µm
 Cytoplasm: cytoplasm is divided into two portion; a clear transparent ectoplasm and a granular
endoplasm. Ingested RBCs, tissue granules and food materials are also found in endoplasm
 Nucleus: It is single, spherical shape and size ranging from 4-6µ Nucleus contains central karyosome
and fine peripheral chromatin.
 Trophozoites are actively motile with the help of pseudopodia.
 Trophozoites are anaerobic parasite, ( present in large intestine)

2. Pre cyst:

 It is the intermediate stage between trophozoite and cyst

 It is smaller in size; 10-20µ
 It is round or slightly ovoid with blunt pseudopodium projecting from periphery
 No RBC or food materials are found on its endoplasm.

3. Cyst:

 It is the infective form of parasite.

 Shape: It is round or round or oval in shape
 Size: 12-15 µm in diameter
 It is surrounded by a highly rectractile membrane called cyst wall. The cyst wall is resistant to
digestion by gastric juice in human stomach
  Nucleus: A mature cyst is quadrinucleated.
 Cytoplasm: Cytoplasm shows chromatid bars and glycogen masses but no RBCs or food particles.
 Mature cyst passed out in stool from infected patient and remained without fouther development in
soil for few days.

Life cycle:

 Life cycle of histolytica is relatively simple and consists of infective cyst and invasive trophozoites
stage.
 Life cycle completes in single host, ie human
 Human get infected with E. histolytica cyst from contaminated food and water. Infection can also
acquired directly by ano-genital or oro-genital sexual contact.

 The mature Cyst is resistant to low pH of stomach, so remain unaffected by the gastric juices.
 The cyst wall is then lysed by intestinal trypsin and when the cyst reaches the caecum or lower part of
illium excystation occurs. The neutral or alkaline environment as well as bile components favor
excystation.
 Excystation of a cyst gives 8 trophozoites. Trophozoites are actively and carried to large intestine by
peristalsis of small intestine. Trophozoites then gain maturity and divide by binary fission.
 The trophozoies adhere to mucus lining of intestine by lectin and secretes proteolytic enzymes which
causes tissue destruction and necrosis. Parasite, when gain access to blood, migrates and causes extra-
intestinal diseases.
 When the load of trophozoites increases, some of the trophozoites stop multiplying and revert to
cyst form by the process of encystation.
  These cysts are released in faeces completing the life cycle.

Pathogenesis:

1. Mode of infection:
 Faeco-oral route
 Ingestion of cyst contaminated foods and water
2. Virulence factors:
i. Cyst wall: cyst wall is resistant to low pH and gastric juice of stomach.
ii. Lectin: Surface of trophozoite contains lectin that is specific to lingards (N-acetyl-galactosamine and
galactose sugar) present in surface of intestinal epithelium.
iii. Ionophore like protein: It causes leakage of ions such as Na+, K+, Ca++ from target cells.
iv. Hydrolytic enzymes: Phosphatase, proteinease, glycosidase and RNase causes tissue destruction and
necrosis.
v. Toxin and haemolysin
3. Pathogenesis;

The parasites express large number of virulence factors including lectin, lytic peptide, cysteine, proteineases
and phospholipase.

Excystation of cyst in intestine releases 4 trophozoites which then colonizes the large intestine. The binding
of trophozoites with the colonic epithelium is a dynamic process in the pathogenesis. After adherence
trophozoite lyse the target cell by its ionophore like protein that causes leakage of ions from cytoplasm. The
proteolytic enzymes secreted by the amoeba causes tissue destruction giving flask shaped amoebic ulcer, is a
typical feature of intestinal amoebiasis.

Trophozoites penetrates the columnar epithelium of mucosa causing lysis and moves deep inside till they
reached submucosa layer and multiply rapidly. Ultimately amoeba destroy considerable area of the
submucosa leading an abscess formation which breaks down to form ulcer. The ulcer is flask shaped with
narrow neck and broad base. The ulcer may be localized in ileo-caecal region or generalized throughout the
large intestine.

From intestine, the parasites may be carried to other vital organs such as liver, heart, brain etc through blood
circulation. Pulmonary and hepatic amoebic abscesses are frequent and rarely cerebral, cutaneous and
splenic amoebic abscesses.

Clinical manifestation:

Infection ranges from asymptomatic to invasive intestinal amoebiasis and extra-intestinal amoebiasis

1. Intestinal Amoebiasis

i. Asymptomatic infection: 90% of E. histolytica infection is mild or asymptomatic

ii. Symptomatic infection
 Non dysentric amoeboic colitis (mild diarrhea)
 Acute amoebic dysentery: it is more common and characterized by abdominal pain, fever and
tenderness. Stool contains RBCs, charcot-leyden crystals and trophozoites.
Complications: toxic megacolon, fulminant amoebic colitis, amoeboma, amoebic peritonitis, perianal
ulceration
2. Extra intestinal amoebiasis:

i. Hepatic infection: non supurative hepatitis, liver abscesses, other complications

ii. Pulmonary infection: chest pain, dyspnoea, non-productive cough
iii. Cerebral infection: it is rare and occurs as a complication of liver of pulmonary amoebiasis
iv. Genitourinary infection: involves kidney and genital organs
v. Spleenic infection
vi. Cutaneous amoebiasis
 Amoebic pericarditis
Lab Diagnosis:
Specimen: stool, pus or liver abscesses, sputum and biopsy samples
i. Stool macroscopy: in amoebic dysentery stool is offensive, semi-solid, fark brown color and acidic in
nature, mixed with blood, mucus and faecal materials.
ii. Microscopy: Normal saline preparation of fresh faecal material revels trophozoites with RBCs in its
cytoplasm and its amoebic motility.
iii. Stool Ag detection: ELISA to detect 170KD lectin of E. histolytica
iv. Stool culture: Robinson’s medium and NH polyxenic culture medium are used to culture E. histolytica
v. Serology: IHA, IFA etc are used to detect antibody in serum against E. histolytica
vi. PCR: It is sensitive test , used to differentiate E. histolytica with other Entamoeba species
vii. Radiological finding: X-rays, MRI, CT scan, ultrasonography etc for extra intestinal amoebiasis..

Treatment and prophylaxis:

 Diloxanide fluorate, diidohyfroxyquin, paramycin, metronidazole, imidazole

 4-aminoquinoline; for extra intestinal infection
 Oral rehydration
 Plasmodium falciparum
Plasmodium falciparum is the most virulent species of Plasmodium in human. It causes malignant tertian or
falciparum malaria. The name ‘falciparum’ is derived by Welch from ‘falx’ meaning sickle or crescent and
‘parere’ meaning to bring forth.

Habitat:

 Various stages of malarial parasites are found inside the parenchymal cellsof liver and inside RBCs
of Human.

Morphology:

Following are the diagnostic forms of parasite found in human

1. Ring form:
o This is the young trophozoite found inside RBCs. The name ring is derived from the
morphological appearance of the stage resembling a ring like structure.
o It consists of central vacuole and nucleus present at the center in the cytoplasm. Often two or
more rings forms of the parasite are found inside a single RBC.
o In stained smear, ring shaped cytoplasm surrounds central blue colored vacuole with red
colored nucleus on it.
2. Trophozoites:
o The trophoizoites ae vacuolated more or less amoeboid and uninucleated.
o They are small, delicate and measures 1.25 -1.5 µm in size
o In a stained preparation, they show a thin ring of blue cytoplasm and darkish stained nucleus.
o In heavy infection, growing forms assume the shape of compact form.
o Single large mass of pigment colored yellow to black called haemozoin are present.
3. Schizonts:
o They are small, immobile, asexual and dividing form of parasite.
rd
o They measure 4.5-5 µm in diameter and occupy about 2/3 of the infected RBC.
o Each schizont contains two or four merozoites and an aggregate of dark stained pigments
o On maturation schizont contains 10-36 merozoites arranged in grape like cluster.
o Each merozoite measure 5-10µm in length.
o Schizonts are very rarely seen in peripheral blood smear. Presence of schizonts in peripheral
blood suggests severe infection.
4. Gametocytes:
o Gametocytes are sexual and erythrocytic stage of parasite and are infectious to mosquitoes.
o They are typically crescent (banana) shape with round or pointed ends.
o Size of mature gametocyte is about one and half time larger than RBC.
o There are two types of gametocytes.
 Microgamete: male form
 Macrogamete: female form

5. Sporozoites:
o The sporozoites are the infective form and are infectious to human
o They are found in infected mosquitoes.
o Sporozoites are single nucleated, sickled shaped structure with equally pointed ends. They
have complex structure and a thick pellicle.
 o Pellicle consists of a thin outer membrane, a two layered membrane and a layer of
subpericular microtubules. They contain 3 polar rings and a mitochondrion present at
posterior end.
o The peripheral fibres serves as organ of locomotion.
o They measures 10-15 µm in length
6. Ookinete and Oocyst:
o They are other form found in infected mosquitoes.

Life cycle of Plasmodium falciparum:

 Malaria parasite shows alternation of generation with alternation of hosts.

1. Intermediate host (Human): asexual cycle take place

2. Definitive host (mosquito): sexual cycle take place

I. Asexual cycle in human host:

 Human gets infected with plasmodium falciparum by the bite of female Anaphelese mosquitoes or
by inoculation of infected blood during transfusion or by congenital route from infected mother to
child.
 In human hosts, two main stages of development is seen. They are;
 o Pre-erythrocytic schizogony in liver
o Erythrocytic schizogony and gametogenesis in RBCs

i. Pre-erythrocytic or primary exo-erythrocytic schizogony:

 This comprises a single cycle and lasts for 6 days.

 Infected mosquitoes during bite inject sporozoites along with saliva into blood vessesls. These motile
sporozoites are carried rapidly withon 30 minutes to the liver by blood stream.
 A protein called circumsporozoite protein covers the surface of sporozoite. It binds specifically and
non-covalently with receptors present on the basolateral area of hepatocyte. Hence sporozoites enter
into liver cell and not into any other cell in human host.
 Within liver cell, sporozoite undergoes a stage of asexual reproduction. During this cycle, sporozoite
are transformed into trophozoites. The growing trophozoite feed on host cell cytoplasm.
 After few days, trophozoites mature and begins schizogony. Numerous daughter nuclei are first
produced subsequently leading to the development of multinucleated liver stage schizonts (EE
schizonts).
 These schizonts are spherical, multinucleated and measures 60µm or more in diameter. They
contains 2000-5000 uninucleated merozoites.
 Mature EE schizonts and liver cell ruptures releasing thousands of merozoites into blood stream.
 Secondary exo-erythrocytic schizogony is absent in falciparum infection.

ii. Erythrocytic schizogony:

 Merozoites releasing from liver cell attach and invasion erythrocyte and begins erythrocytic
schizogony.
 falciparum does not shows any special affinity for any particular type of RBC but invade both
reticulocyte and erythrocyte (young and old).
 The merozoites become attached to the glycoprotein and other sialoprotein on surface of red cell.
 The nature of haemoglobin and red blood cell enzymes influences the development of merozoites
inside RBCs. Development of falciparum is suppressed in presence of fetal haemoglobin and also in
presence of other few haemoglobin.
 Indide RBc, merozoites develops into young trophozoites or ring form. They feed on haemoglobin
by ingesting red cell cytoplasm.
 The trophozoites multiplies by mitosis to become mature schizonts.
 A mature schizont is less symmetrical and contains 8-32 merozoites and haemozoin. Rupture of
schizonts release merozoites into blood circulation. These merozoites within second attach and
penetrate new RBC and begins new erythrocytic schizogony.
 Erythrocytic schizogony is completed with 48 hours and always take place inside capillaries and
vascular layer of internal organs. Therefore, in P. falciparum infection schizonts and merozoites are
usually not demonstrated in peripheral blood smear preparation.

iii. Gametogenesis in RBC:

 After two or three erythrocytic schizogony, some of the merozoites instead of developing into
schizonts, invade new erythrocyte and develop into male and female gametocytes.
 These gametocytes develops in RBCs of bone marrow and spleen.
 The specific stimulus for the production of gametocytes is not known. It is believed to be due to lack
of nutrients, accumulation of metabolic or parasitic debris or due to development of immunity.
 The gametocytes are crescent shape with haemozoin granules found in the central part of cytoplasm
surrounding the nucleus. Only mature gametocytes are found in peripheral blood.
 Gametogenesis completes in 96 hours.
 II. Sexual cycle in definitive host mosquito:

iv. Sporogony:

 The process of formation of sporozoite is called sporogony.

 Anopheles mosquitoes during its blood meal from infected person, ingest both the sexual and
asexual forms of parasite along with blood.
 Mature sexual form ie. Gametocytes are only capable of development, rest forms die and digested.
 It has been estimated that in order to infect a mosquito, the blood of human carrier must contain
atleast 12 gametocytes per mm3 of blood and number of female gametocytes (macrogametocyte)
must be in excess to male gametocytes.
o i. Exflagellation:
o In the mid-gut of mosquito, the male gametocytes divides rapidly through a process of
transformation known as exflagellation giving rise to 4-8 thread like filamentous structure,
microgametes.
o An increase in pH caused by escape of CO2 from blood is suggested to be the stimulus for
process of exfalgellation. A single microgametocyte gives rise to 6-8 microgametes.
o The macrogameocyte does not show any flagellation but mature by simple process of nuclear
reduction and extension of polar bodies. A single macrogamete is formed from a single
macrogametocyte.
o ii. Formation of zygote:
o By the process of chemotaxis, microgamete are attracted towards macrogamete. One of the
male gamete attaches to peripheral side of macrogamete and fertilize to form zygote within
20 minutes to 2 hours after blood meal by mosquitoes.
o iii. Formation of Ookinete and Oocyst:
o In the next 24 hrs, the zygote lengthens and matures into Ookinete.
o Ookinete is 11-13 µm in length and 2.5 µm in width. It penetrates gut wall where it secrete a
thin wall and grows into a spherical structure known as Oocyst.
o Oocyst is spherical 6-12 µm in diameter. It contains single nucleus and pigments granules. As
Oocyst mature, it increases in diameter from 6µm to 60µm and meiosis and mitotic division
follow to form large number of haploid sporozoites.
o iv. Release of sporozoites:
o The oocyst ruptures, releasing sporozoites in the body cavity (haemocoel) of mosquito. The
sporozoites are distributed through the circulating fluids into various organs and tissue of
mosquito except ovaries.
o Sprozoites have special predilection towards salivary glands and ultimately reaches maximum
concentration in the salivary duct.
o Sporogony completes in 9-10 days. The mosquitoes at this stage are infectious and a single
bite can repeats the asexual cycle in human host.

Pathogenesis and pathology of Plasmodium falciparum:

Mode of transmission:

 Human are the only source of falciparum malaria. The infection is transmitted by;
o Bite of infected Anopheles mosquito harboring sporozoites
o Blood transfusion
o Transplacental transmission
o Organ transplantation

Virulence factors:
  i. High level of parasitaemia:
 In P. falciparum malaria, parasite density exceeds more than 250,000-
300,000/ml of blood due to invasion of erythrocytes of all ages.
 30-40% of total RBCs are infected
 ii. Sequestration of parasite:

 Sequestration is the condition of holding back of mature parasites in vital

organs. It is exclusively shown by falciparum due to ability to cytoadherence.
 Inside RBC, P. falciparum merozoites produces a protein within erythrocyte
surface membrane in the form of deformation called knobs. These knobs
produce high molecular weight strain specific adhesive protein. These
proteins in turn mediate attachment of parasite to receptors on endothelium
of capillaries and veins. This causes sequestration of parasitized erythrocytes
in the small post capillaries of internal vital organs especially CNS, kidney,
spleen and lungs
 Cytokines:
 falciparum produces a number of cytokines such as IL-1, TNF and IFN-Ƴ
which are believed to contribute to end organ disease involving the kidney,
lungs and brain.

Pathogenesis of disease progression:

 The clinical symptoms of malaria are primarily caused by the asexual intra eryhtrocytic stage of
parasite. The disease is not caused either by sporozoites, developing stages of parasites in liver,
merozoites releasesd from liver or by gametocytes.
 The diseaseprocess in malaria mainly occurs due to;
o The local and systemic response of host to parasite antigens
o Tissue hypoxia caused by reduced O2 delivery because of obstruction of blood flow by
parasitized erythrocytes
o Anaemia caused by destruction of large number of red cells

 The pathological changes are seen primarily in spleen, bone marrow, liver, lungs, kidney and brain.
The infected organs shows following common features;
o Pigments are present in various organs giving the characteristic slate-gray or black appearance
o The cells of reticuloendothelial system show hyperplasia
o Free pigments, free plasmodia and infected erythrocytes are present within capillaries of
these organs. The capillaries also contains macrophages with infected RBCs and segmented
plasmodia
o Sometimes thrombi caused by aggregation of pigments may also occur in capillaries.

Clinical manifestation and disease caused by Plasmodium falciparum:

 Infection with P. falciparum caused intermittent fever called malaria. The word malaria was derived
from two Italian words ‘mala’ and ‘aria’ meaning bad air.
 falciparum causes falciparum malaria or malignant tertian malaria. It is also responsible for
pernicious malaria.
 Incubation period is 10-14 days.
i. Falciparum malaria:

 Prodromal period:
o The prodromal period varies from a few days to several days. This period includes non-
specific symptoms such as malaise, myalgia, headache and fatigue. Some localized symptoms
such as chest pain, abdominal pain and arthralgia are also seen.
 Malarial paroxysm:
o It is the classical manifestation of acute malaria, characterized by fever, chill and rigor. It
generally starts in afternoon but may starts in nay time.
o Each paroxysm shows a succession of 3 stages;
 Cold stage
 Hot stage
 Sweating stage
o Fever is the key clinical manifestation. Fever occurs every 48 hours which is irregular and
does not shows any distinct periodicity pattern.

Anaemia:

 Anaemia is normochromic and normocytic. It is severe in falciparum infection.

 Lysis of parasitized and-non parasitized RBCs, suppression of erythropoiesis in bone marrow,
increased clearance of non-parasitized RBCs by spleen and autoimmune response are the reason for
anaemia
 Hepatosplenomegaly
 Uncomplicated malaria shows moderate splenomegaly and tender hepatomegaly or even reveal no
abnormalities.

iii. Pernicious malaria:

 The term ‘pernicious malaria’ refers to a series of phenomenon occurring during course of an
infection P. falciparum which, if not effectively treated threatens the life of patients within 1-3 days.
 Severe falciparum malaria may develops into serious complication called pernicious malaria as a
result of capillary blockage.
 Complication occurs in non-immune person, immune-compromised person, pregnant woman and
person with splenectomy.
 Various manifestation of pernicious malaria are;
o Cerebral malaria: hyperpyrexia, coma, paralysis
o Algid malaria; cold and clammy skin with peripheral circulatory failure
o Septicaemic malaria: high temperature, bilious remittent fever, pneumonia, cardiac syncope

iv. Black water fever:

 It is a manifestation of falciparum malaria occurring in previously infected individuals and is

characterized by sudden intravascular hemolysis followed by fever and haemoglobinuria.
 The symptoms is known as black water fever due to dark red to brown-black appearance of urine
because urine consists of free haemoglobin.
 An autoimmune mechanism has been suggested in pathogenesis of black water fever. Eryhtrocytic
autoantibodies produced in previous falciparum infection probably combine with auto-antigen
(infected RBCs) occurring in new infection of erythrocytes with same strain of P. falciparum resulting
in haemolysis of RBCs.
 Clinically this condition is manifests as high fever, vomiting, pain in loin, jaundice,
haemoglobinaemia, haemoglobinuria, circulatory collapse and renal failure.
v. Cerebral malaria:

 The symptoms of cerebral malaria is caused by stagnant hypoxia due to adherence of Parasitized
RBC to endothelium of cerebral venules and capillaries.
 Cerebral malaria is marked by severe headache, high fever, convulsion, changes in mental status and
coma. Death may occurs within few hours

vi. Tropical splenomegaly syndrome (TSS):

 It is also known as hyper reactive malarial spenomegaly. It occurs in some patients living in endemic
areas of Africa, Indonesia and New Guinea.
 TSS is characterized by massive splenomegaly, a moderately enlarged liver with hepatic sinusoidal
lymphocytosis and a marked elevated serum IgM malarial antibodies.
 It is also characterized by absence of malarial parasites in peripheral blood.
 Clinical symptoms includes abdominal mass, dragging sensation of abdomen and sharp abdominal
pain.
 Pulmonary oedema:
 This is the most serious complication of falciparum malaria

vii. Renal failure

viii. Hypoglycaemia with lactic acidosis:

 This condition is associated with quinine treatment.

 Hypoglycaemia results from the reduced glucose supply by impaired hepatic glycogenolysis and
gluconeogenesis and increases consumption of glucose by parasite.

viii. Recrudescence:

 It refers to the occurrence of clinical malaria following the previous attack of falciparum malaria. It
occurs due to persistence of small number of viable merozoites inside RBC in internal organs.
 It is believed to be due to inadequate treatment and frequently seen in drug resistant case, immune-
suppressed and pregnancy.
 It occurs within a few weeks to months of previous attacks.
 Latent malaria:
 It refers to a state of asymptomatic malaria harboring plasmodium gametocytes in peripheral blood.
 These persons are reservoir of malaria and infectious to mosquitoes/
 Other complication:
 Septicaemia, aspiration pneumonia, gastro-intestinal bleeding, diarrhea, secondary bacterial infection
etc.