Advance medical Parasitology study guide November 2019

Prof. Abdul jabbar N. Al-Shammari

Dept. of Medical Laboratory sciences
Faculty of Science/ BUA
• A parasite: “a living organism that acquires some of its basic nutritional requirements
through its intimate contact with another living organism”. Parasites may be simple
unicellular protozoa or complex multicellular metazoa
• Protozoa: unicellular organisms, e.g. Plasmodium (malaria)
• Metazoa: multicellular organisms, e.g. helminths (worms) and arthropods (ticks, lice)
• An endoparasite: “a parasite that lives within another living organism” – e.g. malaria,
Giardia
• An ectoparasite: “a parasite that lives on the external surface of another living
organism” – e.g. lice, ticks
PARASITISM - a relationship in which one of the participants, the parasite, either harms its
host or in some sense lives at the expense of the host
Definitive host: “the organism in which the adult or sexually mature stage of the –
.”parasite lives
one in which the parasite reaches sexual maturity and where the adult form of the parasite
usually resides or in which sexual stages of reproduction occur.
You can think of a definitive host as the ''final'' host for the parasite.
Example: They will be laid as eggs in the grass, something like a sheep will eat that grass and
become infected, and then perhaps something like a wolf will eat the sheep and also become
infected.
In this example; who’s the definitive host?
Intermediate host: “the organism in which the parasite lives during a period of its development
”.only
Now, if that host instead supports a developmental stage of a parasite's life, then we call it
an intermediate host. This type of host serves as a vector for the intermediate stage of the
parasite. Also, we can say that - one in which the immature or larval form

:Example

trypanosomes, the cause of sleeping sickness, humans are the intermediate host, while the tsetse
fly is the definitive host, given that it has been shown that reproduction occurs in the insect. 

Difference Between Intermediate Host and Definitive Host

The key difference between intermediate host and definitive host is that intermediate •
host is the organism in which a parasite lives shortly and passes several asexual

1|Page
stages whereas definitive host is the organism in which a parasite becomes mature
.and reproduces sexually
• A paratenic host is similar to an intermediate host, only that it is not needed for the
parasite's development cycle to progress. Paratenic hosts serve as "dumps" for non-
mature stages of a parasite in which they can accumulate in high numbers.
paratenic (transport) host?

• carries immature parasite

• no development occurs
• host may spread it over distances

Vector: “a living carrier (e.g.an arthropod) that transports a pathogenic organism from an
infected to a non-infected host”. A typical example is the female Anopheles mosquito that
.transmits malaria
What's the difference between biological and mechanical vectors?
Biological vectors Mechanical vectors
parasite uses vector for life cycle changes no life cycle changes go on and the vector
is just used to transport the parasite

haematophagous athropodes such

as mosquitoes and other biting
insects flies for transport of amoebal cysts

What is the difference between a facultative and an obligate parasite?

 facultative parasite: may or may not be parasitic

 obligate parasite: always parasitic (can only exist as a parasite)

 Reservoir host - any animal that harbors an infection that can be transmitted to
humans, even if the animal is a normal host of the parasite
 What's the difference between direct and indirect life cycles?
o direct: parasite needs only one host
o indirect: intermediate host required (requires more than one host)

Methods of infection of parasites (matching)

• faeco-oral (Entamoeba histolytica, Ascaris lumbricoides)
• undercooked food (Trichinella spiralis)
• via arthropod vector (malaria)
• direct penetration (Strongyloides stercoralis,

2|Page
Ancylostoma duodenale)
• direct contact /person to person (Trichomonas vaginalis)
Methods of escape
• faeces
• sputum
• via arthropods
premunition

A. Its intensity and specificity are usually at a lower level than those produced by bacteria and
viruses
B. It refers to non-sterilizing immunity

C. may be protected from super-infection long as the parasites remain in the body
D. its refer as concomitant immunity
E. important in endemic areas in limiting the severity of infection with, e.g. Plasmodium,
Schistosoma diseases.
Latent infection /Toxoplasma gondii
• Malignant alteration /Clonorchis sinensis,Schistosoma haematobium
three Flagellates of the most common and medically significant include:
Giardia lamblia, Trypanosome sp. and
Trichomonas vaginalis
Amoeba –include the pathogenic amoeba Entamoeba and
Endolimax which cause dysentery in humans
Forms and reproduction of protozoa
Cysts - infective forms, survive in the environment
Trophozoites – vegetative forms, capable for reproduction:
Asexual: Schizogony, binary fission,
Sexual: Sporogony, Conjugation
How parasite predominant in one area?
A. Common source of water
B. fields and gardens fertilized by human waste, which could spread the organisms(s) between
groups closely related in their daily routines.
Endemicity
presence of risk factors among the indigenous population and
the presence of reservoirs of infection
as well as vectors for transmitting the organisms, if applicable, lead to pockets of infections

3|Page
Trichinella spiralis cyst seen embedded
in a muscle tissue specimen, resemble cancer may also
occur with some of these virulent organisms
Dehydration from severe diarrhea or anemia related to
parasitic infections also provide important diagnostic information to health care teams
A number of worms caused infections can cause physical trauma by perforating (burrowing) into
the intestines, the circulatory system, the lungs, the liver, or the skin of body
Eosinophilia
An important clinical finding that is sometimes discovered in a common blood test
is found in the CBC.
increase in eosinophils, an increase for parasitic infections may rise to level where
40 to 50 percent of the white blood cells are eosinophils.
Pathophysiology of increased eosinophilia
 Igor mediated eosinophil production is induced by compounds released
by basophils and mast cells, including eosinophil chemotactic factor
of anaphylaxis, leukotriene B4 and serotonin mediated release of eosinophil granules
occur, complement complex (C5-C6-C7), interleukin 5, and histamine (though this
has a narrow range of concentration).
 Harm resulting from untreated eosinophilia potentially varies with cause. During an
allergic reaction, the release of histamine from mast cells causes vasodilation which
allows eosinophils to migrate from the blood and localize in affected tissues.
Accumulation of eosinophils in tissues can be significantly
damaging. Eosinophils, like other granulocytes, contain granules (or sacs) filled with digestive
enzymes and cytotoxic proteins which under normal conditions are used to destroy parasites but
in eosinophilia these agents can damage healthy tissues. In addition to these agents, the granules
in eosinophils also contain inflammatory molecules and cytokines which can recruit more
eosinophils and other inflammatory cells to the area and hence amplify and perpetuate the
damage. This process is generally accepted to be the major inflammatory process in the
pathophysiology of atopic or allergic asthma
MEDICAL CONDITIONS CREATED BY PARASITIC INFECTIONS

 block the intestinal tract or cause hemorrhage if they perforate the intestinal wall.
 liver abscesses; appendicitis; peritonitis; hemorrhagic pancreatitis; anorexia (loss of
appetite); and anemia and vitamin insufficiency related to poor absorption of digested
foods
 steal the victim’s strength and vitality
 iron deficiency,
 abdominal pain, loss of appetite, pica
 protein deficiency, dry skin and hair, skin irritations,
 edema

4|Page
  Advanced cases are characterized by a distended abdomen, stunted growth, delayed
puberty, mental dullness, cardiac failure, and death.

 Trichomonas vaginalis organisms are a class of pathogens that commonly reside in

the vagina of females and the urethra, epididymis, and the prostate gland in males.
 In women there is sometimes a yellowish discharge accompanied by itching and
burning.
 The organism is almost exclusively transmitted sexually and is quite common in
those with multiple sex partners.
 The female will most commonly become aware of the illness first and it is medically
necessary to treat both
Immunity of parasites:
 The immune system may be overwhelmed as parasites are capable of
producing prodigious numbers of offspring on a daily basis.
 These organisms have hijacked the bodies of humans or animals infected by
the parasitic organisms to the detriment of the one infected.
 The immune system may appear depressed
in the presence of infection and this may lead to further damage from bacteria and
virus’s concomitant with the parasitic infection.
DIRECT TESTING FOR PARASITES (Matching?)
A. microscopic examination for either or both ova or more rarely the parasite itself,
B. direct tests for the antigens (usually proteins) of parasites.
C. sputum specimens to examine Entamoeba, roundworm, hookworm, Strongyloides,and
Pneumocystis jirovicii
D. Urine samples are used for testing for certain microfilaria and particularly for
Trichomonas vaginalis infections, blood flukes.

E. Perianal area swabbing to detect pinworm in children

F. Scotch-tape prep of the perianal area obtained before daylight while the child is still
somewhat sleeping.
G. testing specimens against known antibodies
Three of the parasitic organisms have screening tests that measure the presence of antigens
from the parasites by using antibodies formed against the organism.
A. Giardia lamblia, B. Cryptosporidium, C. Entamoeba histolytica
INDIRECT TESTING FOR PARASITES
A. immunological profile of the blood that can be used to indicate some but not all parasites
that may infect humans.
B.determine the presence of antibodies formed against parasitic organisms to confirm the presence
of parasitic pathogens

C. The eosinophil counts

5|Page
 Important notes:
It is necessary to collect a sample of blood at established intervals, such as every 4 to 6 hours for
72 hours around the clock, because some parasites only come out of the tissue in which they
spend most of their time during the middle of the night.
A shortcoming of the procedure that determines the presence of antibodies to the various
parasites are that it would be impossible to determine if the antibodies were due to a past or a
present exposure.
Some parasites may be specific to the blood for certain bodily tissues but the most prevalent
parasites are found in the human intestine.
Due to some parasites that imbed themselves in tissues
where they prefer to live, detection is often not possible
without some sort of invasive procedures.
 Muscle biopsy can reveal the pork tapeworm or trichinella, the latter which migrates into
muscle tissue.
 Rectal biopsy can reveal flukes,
 liver biopsies are used for visceral larva migrants. Hydatid (clear) cysts should have a
biopsy (tissue sample surgically excised) to determine the type of tapeworm that
inhabits the cyst.
 Needle biopsy can show heartworms on rare occasions in the lungs of humans (often a
single worm of Difilaria immitis is found in humans) as well as Pneumocystis jirovec

Intestinal Protozoa - The Amoebae

Entamoeba histolytica
• The ability for Eh to induce amebic colitis and disseminate into
extraintestinal organs depends on the parasite competing with indigenous
bacteria and overcoming the mucus barrier, binding to host cells inducing
their cell death, invasion through the mucosa and outsmarting the immune
system.
The vast majority of those infected with Eh are asymptomatic carriers where the
parasite stays restricted to the lumen of the colon and finally undergoes
.encystment for excretion in stool to carry on the lifecycle
.Eh that have invaded the intestinal mucosa often form flask-like ulcers
Epidemiology - Occurs worldwide; the highest incidence and prevalence is in areas with
.poor sanitation

Pathology and Clinical Manifestations - the most pathogenic of all; causes amoebic
dysentery; can become extra-intestinal; can be fatal. Hepatic abscess is the most
.common and dangerous complication

6|Page
.Chronic infections may last for years; often confused with colitis, cancer

Life cycle divided into two stages

trophozoite—actively
motile feeding stage—food and human blood cells

when environmental conditions are favorable

cyst—dormant, highly resistant, infectious stage

when temperature or moisture levels drop

Replication involves simple binary fission of trophozoite or division

.to produce numerous infectious trophozoites in a mature cyst

Motility—extension of a pseudopod (false-foot) and then drawing

.up the rest of the cell to meet the pseudopod in a “snail like” movement

patients with
diarrhea excrete the trophozoite form which is killed by drying in the environment or
by the acidity of the stomach

asymptomatic
patients excrete infectious cysts that are resistant to drying and
Ingestion of cysts .1
Passage of cysts through the stomach where gastric acid stimulates the .2
release of the infectious trophozoites from the cysts
Trophozoites move to the duodenum where they divide .3
Trophozoites travels to the colon where they attach to colonic epithelial .4
cells
After attachment they produce a cytotoxin that kills epithelial cells so they can gain .5
access to deeper tissues
Continue to divide in colon where amoeba/cysts are excreted in stool OR .6
Trophozoites invade the deeper mucousa and enter the peritoneal cavity .7
Trophozoites are carried in the circulation to the liver but can also be .8

7|Page
carried to the lungs, brain and heart
Clinical diseases of E. histolytica
Amoebic dysentery!!! Related to the destruction of the colonic
.epithelial cells by the organism
Flask shaped ulcerations of the intestinal mucousa with inflammation
Secondary bacterial infection
symptoms:
abdominal pain, cramping passage of numerous
watery and bloody stools
If untreated patients can die of dehydration
Amoeba can invade deeper tissues and enter the blood circulatory
-system where they especially infect the liver as trophozoites are re
.moved from blood as they enter the liver
abscess formation in the liver is common
pain in the liver and elevation of the diaphragm
Entamoeba histolytica Pathology
Extra-Intestinal Lesions and Abscess Occurs

A. Hepatic Amebiasis
B. Pulmonary Amebiasis
Metronidazole—penetrates deeper tissues and destroys amoeba present
.in liver, brain, lungs etc
the organism’s metabolism converts the drug into its lethal form
A second drug is used to eradicate the amoeba present in the intestinal lumen
.(paromomycin)
Tissue Dwelling Amoebae
Naegleria fowleri
an ameboflagellate; a free-living organism alternating between amoeboid and
.flagellated forms; only the amoeboid form is found in tissues
the amoeba gains entry via the nasal mucosa, usually during a swimming event;
it moves along the olfactory nerve, gaining access to the brain via the cribriform
.plate. Cases are invariably fatal. Infections do not spread from person-to-person

8|Page
Naegleria fowleriMeningoencephalitis, irrational behavior, coma & death usually
occur within 9 days of exposure
Amoebae in CSF specimens can be cultured on non-nutrient agar containing
bacteria
.Acanthamoeba spp
Life cycle - also a free-living amoeba. The amoeba reaches the brain hematogenously —
after entering a wound or lesion on the skin. More commonly, the organism is
.associated with getting into eyes via contaminated or homemade cleaning solutions
Symptoms - slow onset (10 or more days). Presents as chronic, granulomatous lesions in
.brain. In eye lesions, the infection resembles a herpes virus infection
.Acanthamoeba keratitis - associated with users of extended-wear contact lenses
Giardia lamblia
Life cycle - man ingests cysts from fecally contaminated environment; the organism
excysts in the upper intestine; trophozoites multiply and attach to the intestinal mucosa;
.often enter the gall bladder. Trophozoites and cysts are passed in the feces
Diagnosis - identification of cysts or trophozoites in stool specimens or duodenal contents
Giardia lamblia
.diarrhea, foul-smelling, greasy, mucus-laden stools, flatulence, nausea, cramps

Infection initiated by the ingestion of infectious cysts (only 10 are

required for infection
Acid in the stomach stimulates the release of trophozoites from the .2
cyst
Trophozoites are released in the duodenum and jejunum (upper part .3
of small intestines) where they multiply by binary fission
Trophozoites attach to the intestinal villi by means of a sucking disk .4
5. Trophozoites can develop into cysts for survival outside of the host
6. Trophozoites cause an explosive diarrhea such that cysts are released
into the environment
7. Trophozoites remain in the G-I tract and almost never found
elsewhere in the body.
Upon detaching clear impressions from the
Sucking disks are left on the surface of the microvilli

Giardia attached to intestinal microvilli by sucking disks

Cysts are resistant to the amounts of chlorine put in municipal water
systems (2 parts per million) therefore water systems should ALSO
filtrate water

The onset of disease is sudden and consists of

foul-smelling watery
diarrhea (seldom bloody)

9|Page
abdominal cramping
flatulence

‫المطلوب من الجابتر االول‬

Entamoeba histolytica: Host parasite interactions at the colonic epithelium

Outline the factors that why large proportion of EH colonized

individual resist invasion disease?
1. Mucus barrier that forms a bimodal layer above single layer of epithelial cells. This acts to
spatially restrict noxious substances, commensal bacteria and potential pathogens from accessing the
epithelial cells while allowing nutrient flux through.
2. The primary component of this mucus barrier is MUC2 mucin, a tremendously large protein with
branched glycans and the most prominent member of the mucin family within the intestine.
3. This glycosylation protects the mucin molecule from proteolytic degradation and may also act as a
molecular decoy to bacteria or other pathogens that possess adhesins mistaking mucus for a target
cell.
4. Eh pathogenesis is to overcome the mucus barrier to gain access to the epithelial cells. Indeed, Eh
binds to the colonic mucus layer with strong avidity through the Gal/GalNAc lectin, targeting the
abundant galactose and N-acetylgalactosamine residues present on the O-linked sugar side chains of
mucin.
5.The Gal/GalNAc lectin has the highest affinity for multivalent saccharides such as GalNAc39BSA,
however has very high affinity for in vivo conjugates such as mucin and fetuin.
6.Eh possess a variety of glycosidases that may remove branched polysaccharides from mucin or host
cells including sialidase, N-acetylgalactosamidase and N-acetylglucosaminidase.
7.Due to the scarcity of free carbohydrates in the colon and competition with the commensal
microbiota, Eh may turn on a pathogenicity program for scavenging polysaccharides. Since mucin is
the largest source of carbohydrates in the colonic lumen, this would increase the degradation of the
mucus barrier and result in Eh encountering epithelial cells. Indeed, Eh glycosidases present in
secreted components interact with the polysaccharide side chains of mucin.
8. In a transcriptome analysis of virulent versus non-virulent Eh during colonization, the glycoside
hydrolase β-amylase was very strongly associated with invasive trophozoites.
9. Eh lacking this β-amylase was unable to breach the mucus layer and perturb the epithelial
barrier. Additionally, various other genes related to glycosidase and carbohydrate
metabolism were induced in pathogenic Eh following colon invasion. Specifically, N-
acetylglucosamine modifies these sugar moieties on mucin leading to a loss of the
protective functions.
10. Mucin protein degradation occurs via cysteine proteinases present in Eh secreted
components and the resulting degradation products are less efficient at preventing Eh
adherence to host cells.
11. Although EhCP1, EhCP2 and EhCP5 make up more than 90% of the cysteine protease
activity in Eh, the degradation of mucin appears to be predominantly from EhCP5 as
antisense inhibition drastically reduces the proteolytic activity.

10 | P a g e
Figure 1 described the event of pathogenesis of EH.
Entamoeba histolytica interactions with the mucosal barriers (clockwise). During
Eh invasion the parasite degrades the protective mucus layers and evoke mucus
hypersecretion from goblet cells (GC). By interacting with epithelial cells directly,
Eh induces a pro-inflammatory responses driven by NF-B and later perturbation of
the tight junction proteins to stimulate water and ion secretion. The epithelial
barrier is then breached by cytolysis of epithelial cells allowing Eh to migrate in
the lamina propria degrading the extracellular matrix (ECM). Here, Eh interacts
with the immune compartment specifically macrophages where either Eh death
will occur through NO-dependent killing or Eh will establish chronic disease.
Conclusions:
• Upon colonizing the colon of the infected host, Eh likely changes its relationship
within the host from a non-pathogen to pathogen.
• This is likely driven by interaction with the microbial communities and could be
driven by nutrient availability.
• Eh then targets the mucus barrier for degradation using the glycans as a food source
and evoking mucin hypersecretion from goblet cells.
• Upon mucin depletion, Eh contacts the epithelial cells via the Gal/GalNAc lectin
inducing robust pro-inflammatory gene expression, release of chemotaxic factors and
antimicrobial peptides.
• The subsequent cytolysis of the epithelial cells leads to a barrier breach where Eh
migrates into the mucosa. Once reaching the lamina propria Eh induces macrophage
activation, resists neutrophil killing and induces massive pro-inflammatory cytokine
release. The ability for Eh to establish in this niche will ultimately decide if infection
persists or if the host successfully clears the parasite (Fig. 1).

11 | P a g e
 ‫الى هنا من الجابتر االول‬

‫من الجابتر‬
2
Host- Parasites Relationship

establishment of the parasite in its host is referred to as an infection. The outcome of the infection is
.highly variable

It may be(a) sub-clinical latent infection, (b) clinical disease or (c)

carrier（The disease is the clinical manifestation of the infection which shows the active
presence and replication of the parasite causing damage in the host. It may be mild, severe,
.fulminant and in some cases may even cause death of the host

12 | P a g e
The person who is infected with the parasite but without any clinical or sub clinical diseases is

.referred to as a carrier
Host factors
The host factor includes:
1) Nutritional status of the host, whether malnutrition or under nutrition.
2) Immune response to parasitic infection
3) Immune status of the host whether there is immuno-suppression or not.
4) The presence or absence of the co-existing disease or other physiological conditions such as
pregnancy, and
5) The age and level of the immunity at the time of infection.
When making a diagnosis of parasitosis, 4 factors need to be considered:
A. the season and history are consistent with the opportunity and signs of parasitosis;
B. the number of parasites and the parasite species is consistent with the severity of the
disease;
C. the lesions are typical of those caused by the parasite species; and
D. the clinical signs are consistent with the pathogenetic mechanisms of the parasite.
• Definitions of virulence as the potential to kill the host and is measured simplistically as
mortality rates or the minimum numbers of parasites that cause host death.
• Parasites dependent on the ingestion of prey (the intermediate host) for transmission will cause
greater pathology in the prey (so that it will be caught and eaten) than in the final host (e.g.
cestode parasites with metacestode stages in one or several prey species).
• • Parasites which have relatively immobile intermediate and final hosts will produce more
equivalent pathology in both. Examples include trematode infections in snails and ruminants.
• Microbial virulence factors have been defined as “products that permit a pathogen to cause
disease” or “components that when specifically deleted [by “gene knock-out” or genetic
mutation] impair virulence but not viability” .
In an analogous fashion, the genetic and proteomic basis of virulence in parasite strains has been
investigated to find targets for vaccines or chemical attack.

Intracellular protozoa: Plasmodium (Malaria)

MALARIA
P. falciparum (most common)
P. vivax
P. ovale
P. malariae
Life Cycle
transmitted by Anopheles mosquitoes

13 | P a g e
sporozoites injected with saliva…. sporozoites invade liver cell undergo an asexual
replication merozoites produced hypnozoites and relapses in Pv and Po
merozoites invade RBCs repeated rounds of asexual replication6-30 merozoites formed
some merozoites produce gametocytes, gametocytes infective for mosquito
fusion of gametes in gut, sporogony on outside of gut wall

asexual replication sporozoites invade salivary glands due to the blood stage of the
infection

no symptoms during liver stage (~ incubation period)

characterized by acute febrile attacks (malaria paroxysms)
periodic episodes of fever alternating with symptom-free periods
manifestations and severity depend on species and host status, acquired
immunity, general health, nutritional state, genetics

paroxysms associated with synchrony of merozoite release

or 72 hr cycles 48
release of antigens, etc
TNF-a
temperature is normal and patient feels well between paroxysms
falciparum may not exhibit classic paroxysms
continuous fever
paroxysms become less severe and irregular as infection P. falciparum expresses ‘knobs’
on the surface of infected erythrocytes. Knobs mediate cytoadherence to endothelial
cells progresses
Falciparum Complications
sequestration of Pf-infected erythrocytes
immune evasion
primarily in brain, heart, lungs, and gut
:leads to complications
cerebral malaria
consciousness ranges from stupor to coma, convulsions frequently observed
onset can be gradual or sudden
Pathophysiology

cytoadherence

cerebral ischemia

,hypoxia

metabolic effects, cytokines (eg, TNF-a)

14 | P a g e
¯

coma

Death

•Blood stages are responsible for the pathogenesis of malarial symptoms with intermittent
fever paroxysms accompanying the synchronous lysis of erythrocytes at 48-72 h intervals
and high levels of host TNF-x and progressive anemia. Organ-specific symptoms may
also occur in chronic infections of the liver and brain.
Malaria Diagnosis

.symptoms: fever, chills, headache, malaise, etc

history of being in endemic area

splenomegaly and anemia as disease progresses

microscopic demonstration of parasite in blood smear (distinguish species)

thick film: more sensitive

thin film: species identification easier

repeat smears every 12 hours for 48 hours if negative

’antigen detection ‘dipstick

ParaSight-F, OptiMal, etc

Why does malaria go to the liver?

After arriving in a human body when an infected mosquito bites, malaria parasites head to
the liver. Here, they change into a new form that can infect red blood cells, and begin to
reproduce. But how the parasites evade the immune system while travelling from the liver to the
blood has eluded scientists until now
What is Erythrocytic Schizogony?
Schizogony is the process of asexual reproduction during which the nucleus undergoes
division preceding cell division. Schizogony produces daughter cells known as merozoites,
which can develop in to gametocytes or enter new host cells and undergo another cycle
of schizogony

Cases:
1. A 44-year-old, returns home to New York following a 2-week camera safari to East
Africa. She started chloroquine anti-malarial prophylaxis 2 weeks prior to her departure
for Kenya and continued throughout her foreign travel. She stopped taking the pills on her

15 | P a g e
arrival home because they made her nauseated. Two weeks after her return she develops
paroxysmal fever and diaphoresis and is quickly hospitalized with febrile convulsions,
jaundice, and anemia. Blood smears reveal red blood cells multiply infected with delicate
ring-like trophozoites and rare sausage-shaped gametocytes. The stage of the parasite life
cycle that is responsible for the appearance of the parasites 2 weeks after departure from
the malarious area is the

• Assay question: A common theme among the various dissimilar

helminth species includes their capacity to strengthen both innate and
adaptive immune regulatory circuitry. In addition, different helminths
may influence different pathways. discuss the evidence for helminth–
host interactions that prevent or control immune-mediated disease.

16 | P a g e