Phylum Apicomplexa

 Class Aconoidasida
 Order Haemosporida
(Blood species)
- Plasmodium vivax
- Plasmodium ovale
- Plasmodium malariae
- Plasmodium falciparum
- Plasmodium knowlesi
 Order Piroplasmida
(Blood species)
- Babesia microti and B. divergens

 Class Sporozoa
(Intestinal species)
- Cystoisospora
- Sarcocystis spp.
- Cyclospora
- Cryptosporidium spp.
Pathogenesis
(Tissue species)
 Cryptosporidiosis:
- Toxoplasma gondii
- Diarrhea
Coccidia - Fever
- Nausea
 largest group of apicomplexans - Vomiting
 a subclass of microscopic, spore-forming, single-celled obligate - Weight loss
intracellular protozoan - Abdominal pain
 opportunistic infection in immunocompromised and - Malabsorption
immunodeficient individuals.  Liver, bile duct, gall bladder  acute and gangrenous
 Life cycle: alternation of sexual and asexual multiplication. cholecystitis
 Infect intestinal tract  Respiratory infection  chronic coughing, dyspnea,
 Provided with secretory organelles: bronchiolitis, and pneumonia
 Rhoptries Diagnosis
 Micronemes  Stool exam - Sheather’s sugar floatation
 Polar rings w/ microtubules  FECT
 Kinyoun’s modified AFB w/ oocysts appearing red-pink
Sporozoa: Intestinal Species doughnut-shape circular organisms in blue background.
Cryptosporidium spp.  Intestinal biopsy material
 C. parvum  Sputum, transbronchial and broncheo-alveolar lavage
 C. hominis  IFA, EIA, and DNA probes specific for C. hominis
 AFB staining
Parasite Biology  Entero test
 All stages of development - GIT of the host.  Merozoites and gametocytes - only recovered in intestinal
 Oocysts - infective biopsy material
 Shape: round Mode of Transmission
 Size: 4 to 5 mm  Swimming in contaminated recreation water
 No. of sporozoites: four (small)  Water or food contaminated with infected feces
 No. of sporocysts: none  Person-to-person transmission
 Other features: thick cell wall; 1 to 6 dark granules  Infected food handlers (beverages, raw vegetables,
may be visible and other food that may be eaten raw)
 Schizonts and Gametocytes  Unpasteurized milk, freshly pressed apple cider, potato salad,
 Schizonts containing 4 to 8 merozoites and sausages
 Microgametocytes Epidemiology
 Macrogametocytes  Worldwide distribution
 Size: 2 to 4 mm  Immunocompromised persons (AIDS), immunocompetent
 Not seen in patient samples children, children in daycare centers, animal handlers
 Phil. – 2.6% prevalence rate
Life Cycle
 thin-walled oocysts infect other enterocysts  autoinfection Treatment
 thick-walled oocysts - passed out with the feces  Spiramycin
 DFS - oocysts
concentration techniques and Kinyoun’s AFB
Prevention and Control
Safranin staining and microwave heating
 Proper treatment of water supplies PCR - to differentiate Cyclospora from closely related Eimeria
 Handling known infected material using gloves species.
 Wearing a gown Treatment
 Proper hand washing  not necessary if symptoms are mild
 Properly disinfecting potentially infected equipment  trimethoprim-sulfamethoxazole - drug of choice.
 full-strength commercial bleach  No other alternative treatment if the patient is unable to
 5 – 10% household ammonia tolerate sulfamethoxazole.

Mode of Transmission
 Contaminated water
Cyclospora cayetanensis  No animal reservoirs have been found and, therefore,
cyclosporidiosis is presently considered mainly as a human
 originally called cyanobacterium-like body. disease.
 Oocysts: similar to Cryptosporidiosis Prevention and Control
 Size: 7 to 10 mm  Good sanitary practices
 No. of sporocysts: two  Water treatment before consuming like boiling since
 Contents of sporocysts: each contains two sporozoites chlorination is not effective.
 Fruits and vegetables should be washed w/ clean water,
Life Cycle
but it would be prudent to avoid eating fruits and vegetables
 ingestion of sporulated oocyst  start the life cycle that have been exposed to natural untreated water.
 released sporozoites invade the epithelial cells of the small
intestines (jejunum)
 Sporozoites  asexual reproduction  numerous merozoites Cystoisospora belli
 Sporozoites  sexual reproduction  gametocyte production  Causative agent of cystoisosporiasis.
 Micro- and macrogametocytes unite  oocysts  sporulated oocyst contains two sporocysts each containing
 Infected humans pass immature oocysts four sporozoites (infective stage).
 oocysts undergo complete sporulation within 7 to 12 days in a
warm environment. Life cycle:

 like other coccidians

 Sporulation occurs
48 hrs after passage
w/stool.

Pathogenesis
 Immunocompetent - infection is asymptomatic, or self-
limiting gastroenteritis.
 severe infections - severe diarrhea and fat malabsorption
Pathogenesis  Symptoms: low-grade fever, anorexia, vomiting, general
body-malaise, weight loss, and flatulence.
 malaise and low-grade fever, occur 12 to 24 hrs after exposure
 Stools usually contain undigested food, mucus, and
 Chronic and intermittent diarrhea occurs early in the infection Charcot-Leyden crystals.
and may alternate w/ constipation w/c lasts for 6 to 7 weeks
Diagnosis
w/ 6 or more stools per day.
 DFS - oocysts
 D-xylose malabsorption Infection is usually self-limiting and
 Concentration techniques: FECT, ZnSO4, and sugar floatation
immunity may result w/ repeated infections.
Oocysts:
Diagnosis
 Shape: Thin-walled, transparent, and ovoid in shape
  Size: 20 – 33 mm by 10 – 19 mm Pathogenesis
 Oocysts in stained fecal smears (modified Ziehl-Neelsen  2 types:
method: 1.Invasive form (rare) – vasculitis and myositis
 granular red color against a green background. - lymph nodes, muscles, larynx
 Phenol-auramine and iodine staining, Kinyoun’s stain, and 2.Intestinal form – nausea, abdominal pain, and diarrhea
auramine-rhodamine stain are also useful - mild, last under 48hrs  (occasional) severe or even life
 String capsule (Enterotest) may be of value. threatening
Treatment  Symptoms: anorexia, nausea, abdominal pain, distension,
 Asymptomatic infections  managed w/ bed rest and a diarrhea, vomiting, dyspnea, and tachycardia – last 36hrs
bland diet, while symptomatic infections, such as those  Acute fever, myalgias, bronchospasm, pruritic rashes,
occurring in AIDS patients, can be treated w/ trimethoprim- lymphadenopathy, subcutaneous nodules with concurrent
sulfmethoxazole. eosinophilia, elevated ESR, and elevated CK levels – last 5yrs
 Combination therapy w/ pyrimethamine and sulfadiazine  Segmental necrotizing enteritis
Prevention and Control  In these cases, humans are dead-end intermediate hosts.
 Humans - only known hosts of C. belli. Diagnosis
 good sanitary practices, thorough washing and cooking of  Presumptive dx – symptoms and a history of recent
food, and drinking safe water. consumption of raw or undercooked meat
 Stool exam - sporocysts
 Sporocysts of S. hominis - first excreted 14 to 18 days after
Sarcocystis s p p. ingesting beef, and those of
 An intracellular protozoon - infect humans and animals causing  Sporocysts of S. suihominis - excreted 11 to 13 days after
sarcosporidiosis or sarcocystosis ingesting pork
 S. hominis  Fecal flotation wet mount - visualize sporocysts in bright-field
 S. suihominis microscopy
 DH – Humans  Preferred flotation over FECT and other sedimentation:
 IH – Humans (occasional), a dead-end host after accidental ®Flotation method based on high density solutions
ingestion of oocysts incorporating NaCl, CeCl, ZnSO4, sucrose, Percoll, Ficoll-
Hypaque, and other density gradient media
Parasite Biology  Note: Microscopy – cannot distinguished species because
 called zoite; banana-shaped cell (sausage-shaped), w/ a sporocysts of different species overlap in size and shape
pointed anterior end (apical complex), which possesses  Definitive diagnosis - biopsy of infected muscle
micronemes, miscropores, and rhoptries. ® Sarcocysts of S. hominis – microscopic in muscles of cattle
Host cell penetration and creation of an intracellular ® Sarcocysts of S. suihominis – macroscopic in muscles of
environment suitable for parasite growth and development swine
Oocysts:  Sarcocysts are identifiable using H & E stain.
® Shape: oval  PAS (+) – confirmatory staining
® Appearance: transparent  Walls of sarcocyst – used in species dx.
® No. of sporocysts: two  24 wall types in 62 species.
® Size of each sporocyst: 15 to 19 mm by 8 to 10 mm  S. hominis and S. suihominis – wall type 10
® Contents of each sporocyst: four sausage-shaped or banana-  Wall of S. hominis – 6 mm thick, appears radially striated from
shaped sporozoites villar protrusions of 7 mm long
® Oocyst cell wall appearance: clear, colorless, double-layered  Wall of S. suihominis – 4 to 9 mm thick, with villar protrusions
Note: only single or double sporocysts cemented together may be of 13 mm long
visible in stool samples  Recently, PCR amplification of the 18S rRNA was demonstrated
to be useful in distinguishing S. hominis, S. fusiformis, and S.
Life cruzi sarcosysts and oocysts.
Cycle Treatment
 rarely required, often asymptomatic
 Agents that have been used are albendazole, metronidazole,
and co-trimoxazole for myositis.
 Corticosteroids have also been used for symptomatic relief.
Prevention and Control
 Thorough cooking or freezing meat
 Freezing the meat at -5oC for several days
 Boiling of drinking water
 Anticoccidial drugs (calves & lambs) – amprolium, salinomycin
as chemoprophylactic agents
  To avoid infection of food animals, they must be prevented  Other features: hundreds to thousands of
from ingesting the sporocysts stage from human feces in bradyzoites enclose themselves to form a cyst
contaminated water, feeds, and bedding. that may measure 12 to 100 µm in diameter
 In heavy and widespread infestations w/ visible cysts – Life Cycle
condemn whole carcass  Human infection begins when oocysts are ingested via
 In lighter infestations – parts of carcass not affected are passed contaminated food and water w/ cat’s feces, life cycle (same
for human consumption w/ coccidians) continues.
 No vaccines currently available  When the mature oocysts reaches the intestine of new host 
excysts  releases 4 sporozoites  penetrate the lamina
Sporozoa: Tissue Specie propia  gain entry to the lymphatics  spread to the
Toxoplasma gondii different organs, tissues, and fluid of the body.
 Infects humans and many species of animals.
 Infective stages: tachyzoite, bradyzoite, and oocysts.  Following the entry of the sporozoite into a new cell 
 complete life cycle occurs only in members of the cat family - tachyzoite  bradyzoite that form cysts.
definitive hosts.  Tachyzoites are found during the initial and acute stages of the
 It follows a typical coccidian life cycle: schizogony, infection.
gametogony, and sporogony in the intestinal epithelium.  Only these two stages are present in humans and other animal
 extraintestinal stages (asexual stages): tachyzoites and intermediate hosts.
bradyzoites.  Asexual multiplication (endodyogeny) – characterized by the
 Intracellular parasite – nucleated cells including marcophages formation of the plasma membrane by the two new daughter
 Oocysts: parasites, even before the division of the nucleus; this process
 Typical infective form liberate trophozoites.
 Similar to that of C. belli, but smaller  Tachyzoites - transferred from one person to another by
 Shape: round to slightly oval granulocyte blood transfusion.
 Size: 10 to 15 mm long by 8 to 12 mm wide  Tachyzoites - transferred from newly infected mother to fetus
 Other features: transparent oocyst contains two during the first trimester of pregnancy by passing thru the
sporocysts, each with four sporozoites; bordered placental barrier.
by a clear, colorless, two-layered cell wall  Tachyzoites and bradyzoites - transferred by organ transplant
 Tachyzoites: especially bone marrow, and bradyzoites can be acquired by
 Actively multiplying morphologic form eating meat of infected animals.
 Size: 3 to 7 × 2 - 4 µm  Trophozoites
 Shape: crescent-shaped, often more rounded on  Shape: crescent-shaped w/ a pointed anterior and a
one end rounded posterior end.
 No. of nuclei: one  Size: 4 – 8 mm in length by 2 – 3 mm width
 Other features: contains a variety of organelles
Pathogenesis
(mitochondria and Golgi apparatus) that are not
 Toxoplasmosis - asymptomatic as long as the immune system
readily visible
is functioning well
 Bradyzoites:
 Cysts - brain, skeletal and heart muscles, and retina.
 Slow-growing morphologic form
 Clinical manifestations become apparent when the immune
 Size: Smaller than tachyzoites
system in suppressed as in old age, drug-induced
 Physical appearance: similar to that of the
immunosuppression after organ transplantation, or in cases of
tachyzoites, only smaller
AIDS.
 Immunocompromised patients - encephalitis, myocarditis, and
focal pneumonia are among the most common manifestations.
 Stillbirth and abortion - mothers acquire the infection during
the first trimester of pregnancy
 Babies may exhibit clinical manifestations like chorioretinitis,
epileptic seizures, jaundice, hydrocephaly, and microcephaly.
 Death of the infected newborn babies is usually due to anemia
w/ pneumonia.
 There are cases where clinical manifestations may not be
apparent during the neonatal period, but will appear later in
childhood as they grow up when their immune system is
suppressed and reactivation of chronic toxoplasmosis.
Diagnosis
 Examination of cysts in tissue imprints stained w/ Giemsa and
H & E stain.
 Serodiagnostic methods - detect antibodies against T. gondii
 ® a seroconversion to a positive titer or a four-fold  In addition, there is one species that naturally infects
increase in titers is indicative of an infection. macaques (primate) which has recently been recognized to be
 Sabin-Feldman methylene blue dye test - very sensitive and a cause of zoonotic malaria in humans.
specific but requires the maintenance of live organisms in the  species infecting humans:
laboratory. - P. falciparum
 High titers - >1,024 - P. vivax
 IgM antibody detection: - P. ovale
 IgM IFAT - P. malariae
 Double sandwich IgM enzyme immunoassay - P. knowlesi
® To differentiate between acute and chronic cases  are pigment producers and are ameboid in shape, w/ some
being more ameboid than the others.
 Other tests: indirect HA, IFAT, ELISA, and Latex agglutination  Asexual cycle – occurs in man
 Differentiating pre-existing Ab from passively transferred Ab  Sexual cycle – occurs in mosquito
from mother or Ab related to illness, is important in the P. falciparum
assessment of serological test results.
 causes severe malaria because it multiplies rapidly in the
 PCR has been successful in the dx of toxoplasmosis. blood, and can thus cause severe blood loss (anemia).
® Samples taken from patient – serum, amniotic fluid, CSF, - clog small blood vessels.
and BAL - when it occurs in the brain, cerebral malaria results, a
Treatment complication that can be fatal.
 Pyrimethamine (25-100 mg daily) and sulfadiazine (1-1.5 g four
P. vivax
times daily) - used in combination for 1 month
 (as well as P. ovale) has dormant liver stages (“hypnozoites’)
® since pyrimethamine can lower blood counts, leucovorin
that can activate and invade the blood (“relapse”) several
(folic acid) should also be given together w/ this drug.
months or years after the infecting mosquito bite.
 Sulfadiazine - cause serious allergic reactions like fever and
P. ovale
rash, it can be substituted w/ clindamycin, spiramycin,
 biologically and morphologically very similar to P. vivax;
azithromycin, clarithromycin, dapsone, and atovaquone.
differently from P. vivax, it can infect individuals who are
 Corticosteroid are sometimes given to prevent occurrence of
negative for the Duffy blood group; this explains the greater
hypersensitivity rxn.
prevalence of P. ovale.
 Prophylaxis w/ Trimethoprim-sulfamethoxazole
P. malariae
Prevention and Control
 the only human malaria parasite species that has a quartan
 Food - protected from contamination w/ cat feces
cycle (three-day cycle). (The three other species have a tertian,
 Meat and eggs - well cooked.
two-day cycle.)
 Unpasteurized milk should be avoided.
- If untreated, P. malariae causes a long-lasting, chronic
 Pregnant women should avoid contact w/ cats.
infection that in some cases can last a lifetime.
 Laboratory workers should be very careful in handling the
- In some chronically infected patients P. malariae - cause
parasite (live trophozoites)  accidental infection.
serious complications such as the nephrotic syndrome.
P. knowlesi
 has a 24-hour replication cycle and so can rapidly progress
from an uncomplicated to a severe infection; fatal cases have
MALARIA been reported; is found throughout Southeast Asia as a natural
Class Aconoidasida: Order Haemosporida: blood species pathogen of long-tailed and pig-tailed macaques. It has
P l a s m o d i u m s p p. recently been shown to be a significant cause of zoonotic
malaria in that region, particularly in Malaysia.
 Malaria remains the leading parasitic disease that causes
mortality worldwide. Causative Agents
 caused by malaria parasites which are micro-organisms that
belong to the genus Plasmodium that is transmitted by the bite
of an infected female mosquito belonging to the genus Plasmodium Species Human Infection
Anopheles. Plasmodium vivax Benign tertian malaria
 characterized by cycles of shaking, chills, fever, sweating, and
anemia. Malignant tertian/ Pernicious
 Affects 500 million and kills more than 1 million people each Plasmodium falciparum
malaria (most common and fatal)
year. Complications: Cerebral Malaria
 Endemic tropical and sub-tropical regions – Sub-Saharan and Black Water Fever
Africa, Asia, and Latin America.
Plasmodium malariae Quartan Malaria
 more than 100 species of Plasmodium, which can infect many
Plasmodium ovale Ovale tertian malaria
animal species such as reptiles, birds, and various mammals.
 Four species of Plasmodium have long been recognized to
infect humans in nature. Life Cycle
 Has 2 stages:  P. malariae – 3 to 4 weeks
1. Sexual phase in the mosquito  The incubation period (the time between sporozoite injection
2. Asexual Phase in the mosquito and the appearance of clinical symptoms is typically 8 to 40
a. Exoerthrocytic (Pre-erythrocytic) shizogony days, depending on species.
b. Erythrocytic shizogony  P. falciparum – 8 to 15 days
 The infectious stage of malaria – sporozoite  P. vivax – 12 to 20 days
(found in the salivary glands of female mosquitoes)  P. ovale – 11 to 16 days
 asexual cycle (humans) - consists of schizogony  merozoites,  P. malariae – 18 to 40 days
and gametogony  gametocytes.  The incubation period may range from 9 days to 3 years,
 sexual cycle (mosquito) - involves sporogony  sporozoites. depending on the:
 The life cycle of all human species of malaria are similar. 1.Parasite strain

2.Dose of sporozoites inoculated

3.Immune status of the host
4.Host’s malaria chemoprophylaxis history
 Any person who has traveled to a malaria-endemic area must be
considered at risk of developing malaria up to 2 years and even
longer upon leaving the area
 When the parasite develops in the erythrocyte, numerous
known and unknown waste substances such as hemozoin
pigment and other toxic factors accumulate in the infected red
blood cell.
 These are dumped into the bloodstream when the infected cells
lyse and release invasive merozoites.
 The hemozoin and other toxic factors such as glucose phosphate
isomerase (GPI) stimulate macrophages to release tumor
necrosis factor (TNF), and other cells to produce cytokines and
other soluble factors which act to produce fever and rigors and
probably influence other severe pathophysiology associated with
malaria.

The classical (but rarely observed) malaria attack lasts 6-10 hours. It
consists of
® a cold stage (sensation of cold, shivering)
® a hot stage (fever, headaches, vomiting; seizures in young
children)
® and finally a sweating stage (sweats, return to normal
temperature, tiredness).
® Classically (but infrequently observed) the attacks occur
every second day with the "tertian" parasites (P.
falciparum, P. vivax, and P. ovale) and every third day with
the "quartan" parasite (P. malariae).
 More commonly, the patient presents with a combination of the
following symptoms:
- Fever
- Chills
- Sweats
- Headaches
Pathogenesis - Nausea and vomiting
 wide variety of symptoms, ranging from absent or very mild - Body aches
symptoms to severe disease and even death - General malaise
 categorized as uncomplicated or severe (complicated)  Physical findings may include:
 All the clinical symptoms associated with malaria are caused - Elevated temperatures
by the asexual erythrocytic or blood stage parasites. - Perspiration
 The prepatent period (the interval from sporozoite injection to - Weakness
detection of parasites in the blood) of malaria is species- - Enlarged spleen
dependent, may range from 11 days to 4 weeks. - Mild jaundice
 P. falciparum – 11 to 14 days - Enlargement of the liver
 P. vivax – 11 to 15 days - Increased respiratory rate
 P. ovale – 14 to 26 days
  Severe malaria occurs when infections are complicated by Lariam
serious organ failures or abnormalities in the patient's blood or Fansidar
metabolism. The manifestations of severe malaria include:  Treatment is dependent on several factors, including:
 Cerebral malaria, with abnormal behavior, impairment of - Type of malaria
consciousness, seizures, coma, or other neurologic abnormalities - Drug-resistance
 Severe anemia due to hemolysis (destruction of the red blood  Nearly all strains of P. falciparum are now chloroquine
cells) resistant, in addition to developing resistance to nearly all
 Hemoglobinuria (hemoglobin in the urine) due to hemolysis other currently available antimalarial drugs
 Acute respiratory distress syndrome (ARDS), an inflammatory  P. vivax has also developed resistance to chloroquine and
reaction in the lungs that inhibits oxygen exchange, which may primaquine, though they are not as widespread as falciparum
occur even after the parasite counts have decreased in response
to treatment
 Abnormalities in blood coagulation
 Low blood pressure caused by cardiovascular collapse
 Acute kidney failure Prevention & Control
 Hyperparasitemia, where more than 5% of the red blood
Epidemiology:
cells are infected by malaria parasites
 The five provinces having the highest number of malaria
 Metabolic acidosis (excessive acidity in the blood and
cases as of 2013
tissue fluids), often in association with hypoglycemia
1. Cagayan
 Severe malaria is a medical emergency and should be
2. Isabela
treated urgently and aggressively.
3. Palawan
Malaria Relapses
4. Sulu
 In P. vivax and P. ovale infections, patients having recovered
5. Tawi-Tawi
from the first episode of illness may suffer several additional
 Malaria can also be transmitted through blood transfusion from
attacks ("relapses") after months or even years without
infected donors, and by contaminated needles and syringes.
symptoms. Relapses occur because P. vivax and P. ovale have
 Early dx and prompt treatment of malaria are essential for
dormant liver stage parasites ("hypnozoites") that may
malarial control.
reactivate.
 Breeding sites of Anopheles should be detected early and
 Recrudescence occurs when the blood schizonticide does not
contained.
eliminate all parasites from the blood stream, either because
 Personal protection measures:
the dose was inadequate or because the parasite is resistant to
- Wearing of light-colored clothing w/c cover most of the body
the drug. (only P.f and P.m.) – due to the remnant of parasites
(since dark colors attract mosquitoes).
in RBC.
- Using insect repellants containing DEET (N,N-diethyl-m-
Diagnosis
toluamide) on exposed body parts.
 Microscopy – "gold standard" for malaria diagnosis
- Use of permethrin insecticide as repellant spray for clothing.
- thick and thin blood smears stained with Giemsa, Wright,
- Proper vector control
or Wright-Giemsa stains.
- Chemoprophylaxis
- Giemsa is the preferred stain, as it allows for detection of
- Using insect spray containing pyrethrum in living areas
certain morphologic features (e.g. Schüffner’s dots,
Maurer’s clefts, etc.) that may not be seen with the other
two.
Class Aconoidasida: Order Piroplasmida: Blood species
 thick smears - detect the presence of parasites
 thin smears are used for species-level identification. B a b e s i a s p p.
 Quantification - both thick and thin smears  Babesia spp. are hemosporidian parasites that cause
 Specimens may be taken any time and all blood stages of the babesiosis, a hemolytic disease commonly referred to a tick,
parasite may be found. splenic, redwater, Texas, or Nantucket fever.
 In falciparum malaria, only the ring & gametocytes are found.  are generally specific to their vertebrate hosts, and are
 Obtaining smears every 6 to 8 hrs. is usually appropriate. transmitted by Ixodidae or hard ticks.
 Rapid diagnostic tests (RDTs)for malaria are already available.  In humans, transmission through blood transfusion, organ
transplantation, and transplacental route have been
 Serological tests: IHA, IFAT, and ELISA, however, tests cannot
documented.
differentiate between current and past infections, but helpful
in epidemiologic studies.  While more than 100 species have been reported, only a few
have been identified as causing human infections, including B.
 PCR
microti, B. divergens, B. duncani, and a currently un-named
strain designated MO-1.
Treatment
 Treatment focuses on eradication of the blood parasite
Parasite Biology
Chloroquine
 requires mammals as primary hosts, and ticks as intermediate
Quinine
hosts or vectors.
Doxycycline
Malarone
  Although hard ticks are the known biological host, soft tick has  drug combination of clindamycin and quinine, or azithromycin
also been reported. and atovaquone
 Unlike Plasmodium, Babesia does not undergo exoerythrocytic
merogony; daughter progeny is not housed in parasitophorous Prevention & Control
vacuoles; and residual bodies are usually nonexistent in  Avoiding tick-infested areas
infected RBCs.  Remaining covered w/ clothing
 Immediately removing any attached ticks.
Life Cycle  application of bug repellents in clothes
 Babesia life cycle undergoes three developmental phases:  rodent population control - major carriers or reservoirs of the
 In the mammalian host: parasite
1.Merogony in the RBCs; and in the tick vector  associated w/ splenectomized and immunocompromised
2.Stages of gamogony in the gut and epithelium, and patients, and noteworthy are the cases acquired through
3.Sporogony accompanied w/ multiple fission in various cells blood transfusion and organ transplantation.
and organs forming sporokinetes, and the development of  inclusion of screening procedures for B. microti for blood and
infective sporozoites. organ donors in high-risk areas.

Pathogenesis
 Most infections - asymptomatic
 Manifestations of disease include fever, chills, sweating,
myalgias, fatigue, hepatosplenomegaly, and hemolytic anemia.
 Symptoms typically occur after an incubation period of 1 to 4
weeks, and can last several weeks.
 more severe in patients who are immunosuppressed,
splenectomized, and/or elderly.
 Infections caused by B. divergens tend to be more severe
(frequently fatal if not appropriately treated) than those due
to B. microti, where clinical recovery usually occurs.
Diagnosis
 Microscopy - thick and thin blood smears stained with Giemsa
 Repeated smears may be needed.
 Antibody detection are also useful like IFAT.
 Molecular diagnosis is helpful in cases the parasite is
undetectable in blood smears

Treatment