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A. Entamoeba histolytica

  1. Source of infection: cyst passing patient/ asymptomatic carrier. Acutely ill patients donot act as reservoirs as they excrete non-infective trophozoites
  2. Transmission: contaminated food, water
  3. Life Cycle: Completed in single host (Man)
  4. Infective stage (Quadrinucleate cyst) ingested in contaminated food/ water? excysts in caecum? trophozoite with four nuclei liberated? divides by binary fission giving rise to 8 daughter trophozoites? migrate to ileocaecal region? penetrate the muscular mucosa & localize in the submucosal layer of the large intestine? lesion by necrosis & destruction of the tissue? penetrate portal circulation? reach different organs of the body 
    1. Zymodeme analysis: isoenzyme electrophoretic mobility have identified seven potentially and 11 non-pathogenic zymodemes.
      Isolates of E. histolytica from patients with invasive amoebiasis have unique isoenzymes, surface antigens, DNA markers, and virulence properties and are now recognized as distinct species from the non-invasive E. dispar.
    2. Clinical features: Asymptomatic (85-95%), Symptomatic (5-15%)
    3. Symptomatic:
      1. Intestinal amoebiasis (95% of symptomatic cases)
      2. Amoebic dysentery (flask shaped, water bottle, undermined ulcer)
      3. Non-dysenteric colitis
      4. Amoebic appendicitis
      5. Amoeboma
Extra Edge :

Balamuthia mandrillaris is a free living amoebae with branching pseudopodia & like acanthoamoeba causes focal granulomatous amoebic encephalitis
Sappinea diploidea-another free-living amoeba reported to cause meningoencephalitis


4.  Complications:

  1. Perforation/Peritonitis
  2. Haemorrhage/Obstruction 

5.  Extraintestinal amebiasis (5% of symptomatic cases)

  1. Diet rich in cholesterol & carbohydrate predisposes to invasive amoebiasis. Invasive amoebiasis is three times more common in men than in women, especially of lower socioeconomic status  
  2. Amoebic hepatitis
  3. Amoebic liver abscess (usually solitary, right lobe, superio-anterior, anchovy sauce pus in center)
  4. Pulmonary amoebiasis/
  5. Cerebral amoebiasis/
  6. Cutaneous amoebiasis/
  7. Urogenital tract amoebiasis 

6.  Laboratory diagnosis

a.  Faecal examination:

  1. saline mount (trophozoites with ingested RBCs, erythrophagus trophozoites, pathognomic feature), iodine mount (morphological details of the cyst), permanent mount (iron-hematoxylin, trichrome stain), after concentration (only cysts seen)
  2. Trophozoite: 15-30µm, pseudopodia, eccentrically placed nucleus with central karyosome, inner surface of nuclear membrane lined with chromatin granules, food vacuoles.
  3. Cyst: 15µm, smooth wall, early cyst or precyst shows chromatoid bars, glycogen mass, disappear as cyst matures. Initially uninuclear, mature cyst quadrimaculatae.
    Proctosigmoidoscopy scrapings/ biopsy
    Pus aspirate (only see trophozoites, no cysts seen)

b.  Culture: Craig’s medium, Balamuth’s medium, Robinson’s medium, diamond’s medium


c.   Serological diagnosis: extremely useful for diagnosis of extraintestinal amoebiasis

  1. ELISA- Most sensitive
  2. IHA: 1:256              
  3. Molecular methods: DNA probes
7. Pathogenic free living amoebae

B. Naegleria fowleri- an ameboflagellate

  1. Primary amoebic meningoencephalitis (PAM)
  2. Trophozoite: amoeboid form: 10-35µm, motile by lobopodia; flagellate form: pear shaped, motile by 2 flagella, non-replicating
  3. Cyst: 7-10µm, smooth double cyst wall, not found in tissues
  4. Infective form: Trophozoites (both forms). Usually infect healthy individuals
  5. Source of infection: swimming in lakes & ponds; amoebae invade nasal mucosa? pass through olfactory plate? reach meninges & cause acute purulent meningitis which is rapidly fatal
  6. Laboratory diagnosis: CSF: neutrophilic leukocytosis, detection of trophozoites (no cysts seen), can be cultivated
  7. Serological tests: not useful due to fulminant nature of the disease 

C.  Acanthamoeba spp., A. castellani, A. culbertsoni, A. israelii

  1. Healthy host -- A. keratitis
  2. Immuno def host – Granulomatous Amoebic encephalitis (Subacute or chronic disease with focal granulomatous lesions in brain.
  3. Trophozoite: 15-45µm, acanthopodia, no flagellate form
  4. Cyst: 10-25µm, double walled, also found in tissues
  5. Source of infection: inhalation, ingestion, traumatized skin/ eyes (contact lenses). Chronic disease with prolonged course
  6. Laboratory diagnosis: CSF: lymphocytes, detection of cysts & trophozoites, brain biopsy often required. can be cultivated
  7. Serological tests: important, Immunofluorescence 
D. Giardia intestinalis
  1. Habitat: duodenum & upper jejunum
  2. Trophozoite: vegetative stage, pear shaped (monkey faced appearance), 10-20x6-15µm, convex dorsal surface, 2 axostyles, 2 nuclei, four pairs of flagella. Multiply by binary fission, motile (falling leaf motility)
  3. Cyst: oval, 8-14x6-10µm, four nuclei, axostyle
  4. Source of infection: humans, infective stage is cyst, through contaminated food & water
  5. Life cycle: excystation in duodenum, trophozoites attach to the intestinal villi & multiply by binary fission
  6. Clinical features: asymptomatic, diarrhoea, malabsorption syndrome
  7. Laboratory diagnosis:
    1. Faecal examination: cysts & trophozoites
    2. Duodenal aspirate: trophoziotes (enterotest)
    3. Duodenal or jejuna biopsy
    4. Antigen detection in stool: ELISA, CIEP, immunofluorescence
    5. Antibody detection: ELISA, IFAT 

E.  Trichomonas vaginalis

  1. Only one form: Trophozoite (no cystic stage)
  2. Trophozoite: pear shaped, 10-30µmx5-10µm, 4 anterior flagellae, fifth flagellum moulded as an undulating membrane, Jerky, wobbling or rotatory motility, multiplies by binary fission
  3. Habitat: vagina in females; anterior urethra in males
  4. Mode of transmission: venereal disease
  5. Clinical features: 20% asymptomatic, females: vaginal discharge, foul smelling frothy, itching (strawberry appearance); males: urethritis, balanoposthitis
  6. Laboratory diagnosis:
    1. Wet mount preparation
    2. Stained smear: giemsa, leishman, papanicolaou
    3. Culture: Bushley’s, Feinberg- whittington’s, Roiron’s, Johnson-trussel 
Extra Edge :

Trichomonas hominis is found in the large intestine where it forms a harmless infection. Infection is by a resistant stage.

T. tenax is found in the mouth were it forms a harmless infection. Infection is by direct contact


F.  Trypanosoma spp.

  a.  Trypanosoma brucei gambiense

West African sleeping sickness (western, central parts of Africa)

  1. Trypomastigote: actively motile, spindle shaped
  2. Antigenic variation: shed outer variant surface glycoprotein and replace with another

a.  Life cycle:

  1. Definitive host: man, game, domestic animals
  2. Intermediate host: tsetse fly (glossina palpalis, glossina tachinoides)
    Stumpy trypomastigote in human blood? ingested by fly? multiply in mid gut? migrate to salivary glands? transform into epimastigotes? transform into metacyclic trypomastigotes (EIP: 25-50days) (infective stage for man)? fly bite? transform into slender trypomastigotes? in peripheral circulation? some transform into stumpy trypomastigotes
  3. Reservoir: man only
  4. Clinical features: trypanosomal chancre? febrile attacks, lymphadenopathy (winterbottom’s sign: enlargement of posterior cervical lymph nodes)? CNS involvement (Kerandel’s sign: pressure on palms of the hand or over ulnar nerve is followed by severe pain after pressure is removed)

2.  Laboratory diagnosis:

  1. Trypomastigote: chancre, peripheral blood, bone marrow, lymph node aspirate, CSF
  2. Trypanosoma brucei rhodesiense 

3.  East African sleeping sickness (eastern, central Africa)

  1. Life cycle : morphology, antigenic variation, life cycle similar, (glossina morsitans, glossina pallidepis). Wild game & domestic animals act as reservoir hosts
  2. Clinical features : more rapid & fatal course
G. Trypanosoma cruzi
  1. American trypanosomiasis/ Chaga’s disease
  2. Central/ south America
  3. Trypomastigote form: C shaped, 20µm long
  4. Amastigote form: oval, 2-4µm, nucleus, kinetoplast
  5. Life cycle:
    1. Definitive host: humans, wild, domestic animals
    2. Intermediate host: reduviid bug (kissing bug)
    3. Trypomastigote form? taken up by reduviid bug after biting human? transformed into amastigote in mid gut & multiply by binary fission?  migrate to hind gut? transformed into metacyclic trypomastigotes? excreted in faeces? defecate soon after biting? invade tissue cells? converted into amastigote forms? mutiply by binary fission & after passing through promastigote & epimastigote forms are transformed into trypomastigotes? liberated in the blood.
    4. Clinical features: Romana’s sign (facial swelling, oedema of one eyelid), chagoma, systemic complications (fever, LAP, hepatosplenomegaly), chronic phase (destruction of muscle, nerve cells: cardiac myopathy, megaesophagus, megacolon)
    5. Laboratory diagnosis:
      1. Peripheral blood smear examination
      2. Xenodiagnosis
      3. Culture: NNN medium, warren medium
      4. Lymph node, muscle biopsy: amastigote form
      5. Serological tests: CFT (machado-guerreiro test), IFAT, ELISA 

H. Leishmania spp.

Leishmania donovani
  1. Kala-azar or visceral leishmaniasis
  2. Habitat: amastigote form is found in cells of RE system (liver, spleen, bone marrow). Promastigote form is found in the gut of sand flies (phlebotomus argentipes)
  3. Amastigote: 2-4m, round, oval, kinetoplast (LD body)
  4. Promastigote: 15-20m x 1.5-3.5µm, single flagellum
  5. Mode of transmission: sandfly (phlebotomus), vertical transmission, blood transfusion
  6. Life cycle: blood meal? transform into promastigotes in the gut of the insect? migrate to mouth parts (partial or complete blockage) (EIP:8-20days)? parasites dislodged when blocked sandfly tries to ingest blood? in human convert into amastigote forms? multiply in the RE system.
  7. Clinical features: IIP: 3-6month, fever, hepatosplenomegaly, pigmentation of skin, weight loss 

a.  Laboratory diagnosis:

  1. Nonspecific tests:
  2. Progressive neutropenia with relative lymphocytosis
  3. WBC:RBC (N 1:750) 1:1000
  4. Reversed albumin: globulin ratio
  5. Napier aldehyde test
  6. Chopra’s antimony test
  7. Demonstration of LD bodies: Spleen (most sensitive)> bone marrow> liver> lymph nodes; D/D Toxoplasma gondii, H. capsulatum
  8. Culture:
  • Monophasic media: Grace’s, Schneider’s
  • Biphasic media: NNN, Tobie’s, BHI agar
  • 24°C for 7 days
  • Leishmanin (Montenegro test)-delayed hypersensitivity test. Negative in active disease
  • Detection of the antigen: ELISA, immunofluorescence
  • Detection of the antibodies: CFT, CIEP, IFAT= 1:32, ELISA, Direct agglutination, IHA
  • ELISA using rk39 antigen has been found to have 100% sensitive & 96% specific. It has both diagnostic as well as prognostic importance (antibody titer falls with the successful treatment)

b.  Post kala-azar dermal leishmaniasis:

  1. 2-10% cases of visceral leishmaniasis. Seen in India and Sudan only
  2. Those adequately treated with antimony/ spontaneously cured
  3. Depigmented macules, erythematous patches, nodular lesions
  4. Diagnosis: Biopsy, culture, no role of serology 
2.  Leishmania tropica                        
  1. Oriental sore, Delhi boil, Baghdad boil, Aleppo button or cutaneous leishmaniasis
  2. Central, western India
  3. P. sergenti, P. papatasii
  4. Reservoir: dogs 
3.  Leishmania brasiliensis
  1. Mucocutaneous leishmaniasis (espundia). Not seen in India
  2. Sandfly: Lutzomyia spp.
  3. Reservoir: small rodents
I.   Balantidium coli-Ciliate dysentery
  1. Largest protozoal parasite & only ciliate infecting humans
  2. Habitat: large intestine, caecum, terminal ileum
  3. Reservoir: pig
  4. Trophozoite: 80-120µm, peristome, cytostome, cytopharynx, cytopyge, two nuclei (macronucleus, micronucleus)
  5. Cyst: spherical, ellipsoid, 50-75µm, double layered cyst wall 

1.  Life cycle:

  1. Natural host: Pig, man incidental host
  2. Infective stage: cyst
  3. Transmission: pig to pig, pig to man, man to man, man to pig 

2.  Laboratory diagnosis:

  1. Faecal examination: trophozoite, cyst
  2. Culture 

J.   Plasmodium spp.- Malaria

  1. P. vivax (most common)
  2. P. malariae
  3. P. ovale (Few reports only from Orissa)
  4. P. falciparum (subgenus laverania)
  • P.v, P.f account for 80% of infections
  • Habitat: hepatic parenchymal cells, RBCs
  1. Man: intermediate host
  2. Female anopheles mosquito: definitive host
  3. Human cycle (Schizogony/ asexual cycle): female anopheline mosquito bites? sporozoites injected? general circulation? invade hepatocytes? preerythrocytic schizogony? merozoites? invade RBCs? erythrocytic schizogony? some merozoites develop into gametocytes
  4. P. vivax (Schuffner’s dots), P. malariae (Zeimann’s dots)
  5. P. ovale (Schuffner’s dots), P. falciparum ( Maurer’s dots)
  6. Mosquito cycle (Sporogony/ sexual cycle):  female anopheline mosquito bites? picks macrogametocyte & microgametocyte? exflagellation of microgametocyte? penetrates one macrogamete? zygote? ookinete? penetrates the epithelial lining & muscular wall & lies below the outer limiting membrane of the stomach? oocyst? sporocyst containing sporozoites? rupture, sporozoites liberated in the body cavity? reach salivary gland
  7. In P.v & P.o hepatic forms (hypnozoites) persist & remain dormant and are responsible for relapses
  8. In P.f & P.m there is persistence of erythrocytic stages leading to recrudescence
  9. Extrinsic incubation period: 8-21 days

1.  Intrinsic incubation period:

  1. P.f: 12 days,            
  2. P.v: 14 days
  3. P. m: 28 days,         
  4. P. o: 17 days
  • Clinical features: Fever, anaemia, splenomegaly
  • Complications: Blackwater fever, pernicious malaria, cerebral malaria

2.  In-vivo anti malarial susceptibility testing:

a.  Sensitive: If asexual parasites have cleared by day 6 from the beginning of treatment without subsequent recrudescence until day 28

  1. RI: If asexual parasites have cleared for atleast 2 consecutive days, latest on day 6 from the beginning of the treatment, followed by recrudescence (early, before day 14; late, between days 15 & 28)
  2. RII: showing marked reduction of asexual parasitaemia to less than 25% of the pretreatment count within 48hrs. of the initiation of treatment, but no subsequent disappearance of parasitaemia (positive on day 6)
  3. RIII: Showing only modest reduction, no change, or an increase in asexual parasitaemia, during the first 48 hrs. following the implementation of treatment and no subsequent clearance of parasitaemia  

3.  Laboratory diagnosis:

  1. Peripheral blood film examination: Thick, thin film. Giemsa/JSB stain
  2. Quantitative buffy coat
  3. Antigen detection ( MRDT’s): PfHRP2 (parasight F test), pLDH (Optimal test), Aldolase
  4. Molecular methods: DNA/ RNA hybridization, PCR
  5. Antibody detection: IFAT, IHA

Severe Malaria: Common Clinical Manifestations



Clinical Features


Sluggish flow caused by sticky knobs on parasitized red cells leading to stagnant hypoxia and vascular damage.

Impaired level of consciousness. Hyperpyrexia. Convulsions. Generalized and localized neurological signs.


Destruction of parasitized and nonparasitized red cells by immune complexes, bone marrow suppression and splenic pooling.

Pallor and jaundice. High output cardiac state.


Acute tubular necrosis resulting from sluggish blood flow and hypotension. Hemoglobinuria.

Oliguria. Haemoglobinuria. Acute renal failure.





Increased pulmonary capillary permeability.

Cough. Crepitations, pulmonary edema, iatrogenic fluid overload, bronchopneumonia.


Unknown. ? Partially due to haemodynamic changes.

Jaundice (mainly attributable to haemolysis). Elevated serum enzyme levels, impaired elimination of drugs, prolonged prothrombin time, bleeding.

Fluid and electrolyte balance

Unknown. ? Partially due to inappropriate release of antidiuretic hormone.

Increased intravascular volume. Electrolyte changes, hypoglycemia, hyperkalemia and hemolysis.


Sluggish blood flow in placental vessels leading to vascular damage.

Fetal death. Premature labour.

K. Toxoplasma gondii
  1. Toxoplasmosis
    1. Trophozoite (tachyzoites): crescent shaped, 3x7µm, multiply by endodyogeny, found in tissues during acute stage. Appear rounded enclosed within the host cell (pseudo cyst)
    2. Tissue cyst: formed during chronic infection. Skeletal, heart muscle, brain. 200µm. bradyzoites
    3. Oocyst: found in the definitive host (cat). 10-12µm round. Shed in faeces. Freshly passed contain a single sporoblast. Sporoblast divides into 2 sporocysts & 4 sporozoites develop in each sporocyst (infective form for humans)
  2. Life Cycle:
    1. Enteric cycle: cat; Exocenteric cycle: human, mouse
    2. Enteric cycle: sporozoites released from ingested mature oocyst? penetrate epithelial cells of the intestine? merozoites? some merozoites form tissue cysts in various extraintestinal tissues; some develop into gametocytes? fertilization? oocyst? shed in faeces
    3. Exenteric cycle: ingestion of oocyst, tissue cyst. Only asexual development occurs in man, oocysts are not formed. Merozoites enter lymphatics? blood? tissue cysts in various organs
  3. Mode of transmission:
    1. Contaminated food (oocysts)
    2. Vertical transmission (congenital infection)
    3. Blood transfusion
  4. Clinical features
    1. Congenital toxoplasmosis: chorioretinitis, blindness, epilepsy, mental retardation
    2. Disseminated infection: Immunocompromised (AIDS), CNS involvement (encephalitis, meningitis, SOL)
  5. Laboratory diagnosis
    1. Direct examination: giemsa, immunofluorescence
    2. Animal inoculation: I/P inoculation in mice
    3. Serology:
      1. LA,
      2. Direct agglutination test,
      3. IHA,
      4. ELISA,
      5. CFT,
      6. IFAT,
      7. Sabin & Feldman dye test (specific inhibition by antibody of the staining of trophozoites by alkaline methylene blue)  

L.  Cryptosporidium parvum C. parvum has 2 genotypes, the first of which became known as C. hominis

Other agents that can infect humans include C. felis (feline cryptosporidia), C. muris (rodent cryptosporidia) and C. meleagridis.

  1. Oocyst: 4-5µm, mature contains 2-4 sporozoites, thin walled reinfect the host, thick walled is excreted out
    Transmission occurs fecal-orally, or when oocysts from feces are ingested Chlorination and treated water supplies are not always sufficient to kill Cryptosporidium. As few as 10 to 100 oocysts can initiate an infection.
  2. Life cycle: Completed in one host, infective stage: oocyst? excystation in the small intestine? invade epithelial cells? trophozoite? merozoites? micro & macrogametocytes? zygote?oocyst-> sporulated oocyst which is the form that is seen in stool and is infective for humans. Hence can cause autoinfection
    The parasite is located in the brush border of the epithelial cells of the small intestine, mainly in the jejunum.  When the sporozoites attach the epithelial cells’ membrane envelops them.  Thus, they are “intracellular but extra cytoplasmic 

1.  Clinical features:

  1. Protracted diarrhoea in immunocompromised patients (AIDS), most common cause
  2. There are 4 clinical presentations for patients with AIDS.

i.   4% have no symptoms,                  
ii. 29% have a transient infection,

iii. 60% have chronic diarrhea,             
iv. 8% have a severe, cholera-like infection.

The most severe form results in the patients excreting at least 2 liters of watery diarrhea per day.  They can lose up to 25 liters per day.

  • When the CD4+ count is greater than 200 cells/mm3 the disease is either asymptomatic or resolves on its own.  When the CD4+ count is less than 100 it is chronic and can spread beyond the intestine. 
  • When Cryptosporidium spreads beyond the intestine, as it can predominantly in patients with AIDS, it can reach the lungs, middle ear, pancreas, and stomach.  The parasite can infect the biliary tract, causing biliary cryptosporidiosis.   Result in cholecystitis and cholangitis.   

2.  Reservoir

The main reservoir for Cryptosporidium is domestic animals. Cryptosporidium parvum can reside in 150 different species of mammals such as cattle, sheep, goats, deer, mice and pigs


3.  Laboratory diagnosis:

  1. Faecal examination: wet mount (oocysts), modified ZN staining (5%sulphuric acid, acid fast), IFAT, ELISA,
  2. PCR

Treatment-Spiramycin or Nitazoxanide


  1. Transmission: Cyclosporiasis is spread fecal- orally, through the ingestion of contaminated food or water. However, the disease isn't spread directly from person to person because it requires time to sporulate in the external environment
  2. Infective form-sporulated oocyst.
  3. Oocyst excreted in feces-unsporulated. Sporulates in the environment to become infective
  4. Morphology- Oocysts are round and generally between 8 and 10 microns. They look similar to cryptosporidium oocysts, but are large The oocyst coat of cyclospora is often described as “wrinkled .” Each sporulated oocyst has two sporocysts that each have two sporozoites
  5. Diagnosis: Cyclospora oocysts can be detected by acid fast staining and since oocysts are shed in low numbers, stool samples may need to be concetrated or repeated in order to detect the oocysts.
  6. Oocysts cannot be detected with enzyme immunoassay (EIA) or fluorescent antibody testing, but they do autofluoresce under UV light. PCR (polymerase chain reaction) can also be used to look for C. catayensis DNA in order to diagnose cyclospora infection
  7. e.  Treatment-cotrimoxazole 

N. Isospora

  1. Spread through ingestion of contaminated water or food .
  2. Most incidences of the disease appear in (but are not limited to) tropical regions .
  3. A common cause of diarrhea in immunocompromised
  4. Oocysts (the stage of I. belli that exists in the external environment) are ovoid in shape and measure 20-33 x 10-19 micron
    1. Immature, unsporulated oocyst is excreted through feces.
    2. Sporoblast divides into two.
    3. Each sporoblast develops into a sporocyst with 4 sporozoites, resulting in mature oocysts. The           time   spent in stages 1 through 3 is 2-3 days.
    4. Mature oocyst is ingested.
    5. Oocyst bursts. Sporozoites are released and lodge into the intestinal lining. Sporozoites undergo   asexual reproduction to form merozoites. The merozoites mature into gametes which undergo fertilization to produce a new oocyst 

1.  Diagnosis:

  1. Stool examinations :
  2. Bright field microscopy/UV fluorescence microscopy
  3. Acid-fast stain 

O. Babesia spp.

  1. Babesiosis-disease resembling malaria
  2. Also known as Prioplasmosis
  3. Common names of the disease include Texas Cattle Fever, Redwater Fever, Tick Fever, and Nantucket Fever
  4. Human infection caused by B. bovis, B. divergens, B. microti
  5. Organisms show antigenic variation
  6. Mode of transmission: Ticks. Also contracted from packed red blood cell (PRBC) transfusions and from organ transplantation
  7. Reservoir of infection: ticks (trans-ovarial transmission), mouse, voles and deer
  8. Life cycle:
    1. sexual cycle in insect host (definitive host),
    2. asexual cycle in mammals( intermediate host).
    3. Infective form for humans- sporozoite
    4. Infective form for mosquito-gametocyte
    5. In mammals invades RBCs (Maltese cross-budding merozoites). No malarial pigment
    6. No preerythrocytic stage as seen in malaria

1.  Clinical features:

  1. For 25% of cases in adults and half of cases in children, the disease is asymptomatic or mild with flu-like symptoms.Fever, myalgia, hemolytic anemia, hepatosplenomegaly, and severe infection in splenectomised people.
  2. divergens infections have a much higher fatality rate (42%) and present with the most severe symptoms. Infected individuals suffer from hemoglobinuria followed by jaundice, a persistently high fever, chills and sweats. If left untreated, B. divergens infections can develop into shock-like symptoms with pulmonary edema and renal failure .
  3. Lyme’s disease may co-exist in the same patient

2.  Laboratory diagnosis

  1. Peripheral blood smear examination
  2. Serological diagnosis: IFAT, IHA, ELISA
  • Treatment-quinine and clindamycin

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