Parasitology

Question 1

What is a bloodborne parasite?

Answer 1

1. The parasite can be found in the bloodstream of infected people
2. The parasite might be spread to other people through exposure to an infected person’s blood (for example by blood transfusion or by sharing needles or syringes contaminated with blood).
3. In nature, many bloodborne parasites are spread by insects (vectors), so they are also referred to as vectorborne diseases.

Question 2

Examples of parasitic diseases that can be bloodborne

Answer 2

Malaria,
Babesiosis,
African trypanosomiasis,
American trypanosomiasis (Chaga’s disease),
Visceral leishmaniasis,
and Toxoplasmosis.
-Lymphatic filariasis diagnostic stage (micofilaria) is present
in the blood stream in acute stage of the disease.

Question 3

What is malaria

Answer 3

-Malaria is a life-threatening disease.
-The disease is typically transmitted through the bite of an infected Anopheles mosquito.
-Infected mosquitoes carry the Plasmodium parasite.
-Malaria is typically found in tropical and subtropical climates where the parasites can live.

Question 4

Describe Life cycle of plasmodium

Answer 4

• Lifecycle involves asexual reproduction (schizogony), followed by sexual reproduction (sporogony). This is known as alternation of generations.
• Lifecycle is completed in more than one host (heteroxenous)

It includes:
I.Cycle in man:
* In liver cells: Exo-erythrocytic schizogony.
* In the red cells:
1. Erythrocytic schizogony cycle
2. Gametogony cycle

II.Cycle in the vector: Sporogony cycle

Question 5

Where does malaria usually occur?

Answer 5

Malaria generally occurs in areas where environmental
conditions allow parasite multiplication in the vector.
* Malaria is usually restricted to tropical and subtropical areas
and altitudes below 1,500 m. However, this distribution might
be affected by climatic changes, especially global warming,
and population movements.
* Due to increasing tourism worldwide, an increasing number of sporadic cases in countries outside endemic areas.
* Infected mosquitoes imported by planes can also cause sporadic cases in resident of these countries.

Question 6

What species of plasmodium affect man?

Answer 6

• 1. P. vivax,
• 2. P. falciparum,
• 3. P. malariae ,R.H. Chimpanzee
• 4. P. ovale.
• 5. P. knowlesi a 5th species prevalent in South
     East Asia

Question 7

Habitat of plasmodium

Answer 7

Temporary in liver cells then Red blood cells (intraerythrocytic).

Question 8

Vector (DH) and IH of plasmodium

Answer 8

-Female Anopheles
mosquito (bites between dusk and dawn)
-Man

Question 9

Infective stage to man and mosquitoes

Answer 9

-Sporozoites
-Gametocytes

Question 10

Mode of infection of plasmodium

Answer 10

1) Bite of infected female
Anopheles mosquito.
2) Blood transfusion.
3) Accidental malaria - Common usage of
syringes.
4) Transplacental transmission (congenital malaria) may occur in
endemic areas.
5) Organ transplantation.

Question 11

Describe life cycle of plasmodium –in liver cells–(Exo-erythrocytic schizogony cycle)

Answer 11

• The infective stage is the sporozoite
• It is introduced with the saliva of the biting female Anopheles mosquito.
• It circulates in the blood and then enters the liver cells where it divides and maturate into schizont containing thousands of merozoites.
• Liver cells burst releasing merozoites into circulation

Question 12

Describe Cycle in the red cells: (Erythrocytic schizogony cycle +
Gametogony cycle)

Answer 12

• The liberated merozoites from the liver cells invade red cells but never reinvade liver cells.
• Inside the RBCs, merozoites start division: erythrocytic
  schizogony.
• Erythrocytes rupture and the liberated merozoites reinvade other red cells
• After completing some schizogony cycles, some merozoites do not develop into schizonts but instead male and female sexual stages called gametocytes are formed inside RBCs. This is called gametogony cycle.

Question 13

Describe cycle of plasmodium in vector

Answer 13

1. It takes place in the midgut of the female Anopheles mosquito.
2. All ingested stages are digested except the gametocytes which complete the cycle.
3. Male (micro) gametocytes mature into microgametes by exflagellation, while female (macro) gametocytes mature into macrogametes by reduction division of its nucleus.
   Exflagellation: is the process of maturation of the microgametocyte into microgametes. It occurs in the midgut of the mosquito. The nucleus of the microgametocyte divides into 4-8 fragments by reduction division which migrates into thread like extrusions of the cytoplasm that lash about, and separate as microgametes.

Question 14

How do you identify the plasmodium species?

Answer 14

Species identification:
This is based on:
1.Shape and size of the intra-erythrocytic parasitic stages: trophozoites, schizonts, macro- and micro-gametocytes.

2.Developmental stages in peripheral blood:
* All erythrocytic stages circulate in the blood except in P.falciparum infections where only immature trophozoites (rings) and gametocytes appear in peripheral blood.
Mature trophozoites and schizonts are sequestered in the blood vessels of the internal organs leading to vascular obstruction.
3.Modifications of infected erythrocytes:
– Infected RBCS are enlarged in Plasmodium vivax and Plasmodium ovale.
– In P. ovale the wall of the erythrocyte tends to be weak and acquires an oval shape while spreading the blood film

4.Presence of dots or clefts on the red blood cell(stippling)

Question 15

Describe morphology of plasmodium vivax

Answer 15

Early trophozoite (Ring form)
Ring form with single chromatin dot, thin rim of cytoplasm and a
vacuole.
Size: 1/3 of RBC.

Late trophozoite (amoeboid form)
irregular with amoeboid cytoplasm.

Mature schizont
With 12-24 merozoites, clumped malaria pigment.
Size: fills RBC.

Male (micro) gametocyte
Rounded with diffuse chromatin.
Size: fills RBC.

Female (macro) gametocyte
Rounded with compact chromatin.
Size: fills RBC.

Red cell: enlarged.
Stippling: Schuffner’s dots

Question 16

Describe plasmodium falciparum

Answer 16

-Early trophozoite (Ring form)
-Ring form with 2 chromatin dots,
very thin rim of cytoplasm and a vacuole.
multiple infections (more than one ring) and accolé (marginal) forms.
Size: 1/6 of RBC.

• Late trophozoite with compact cytoplasm.

-Mature schizont with 12-24 merozoites, clumped malaria pigment.
Size: 2/3 RBC.

-Male (micro) gametocyte Crescent with diffuse chromatin.
Size: larger than RBC.

-Female (macro) gametocyte Crescent with compact chromatin.
Size: larger than RBC.
-Red cell: unchanged.
-Stippling: Maurer’s clefts.

Question 17

Describe Malaria

Answer 17

• Malaria is a disease resulting from infection with Plasmodium spp.
• The disease is endemic in more than 90 countries.
• P. vivax is the most common, it accounts for 80 % of cases.
• P. falciparum is the most dangerous (causing malignant malaria), it accounts for 15 % of cases.

Question 18

clinical incubation period (definition and time in malaria)

Answer 18

The time between the inoculation of sporozoites and first appearance of characteristic malaria paroxysm
- It takes 1-5 weeks according to the species

Question 19

Prodromal symptoms of malaria

Answer 19

Early cycles of multiplication cause headache, bone ache and irregular fever. may be misdiagnosed as influenza

Question 20

Malarial paroxysmal attacks (cause and occurrence in each species)

Answer 20

1) Due to rupture of RBCs with release of toxins, parasite debris, malarial pigment and pyrogens.

• Plasmodium vivax and ovale: repeated regularly every 3 days (benign tertian malaria)
  -Relapses may occur every few months
• Plasmodium malariae - repeated every 4th day (quartan malaria)
• Plasmodium falciparum - repeated every 3rd day (malignant tertian malaria)
  -There is no synchronicity in rupture of schizonts.

Question 21

Describe the stages of a paroxysmal attack

Answer 21

Cold stage: (0.5-1 hour):
Patients feel cold, shivering, cold pale skin
temperature is 38 -39 ºC.

Hot stage: (4-6 hours):
Fever, hot dry skin, flushed face, patients
become irritable; temperature is 40 - 41 ºC.
Convulsions may occur in children.

Sweating stage (1-2 hours)
Profuse sweating, fever subsides, patients become exhausted

Question 22

Describe Malignant Malaria (cause for severe infection

Answer 22

1) Infection is usually severe due to sequestration of RBCs

• Sequestration occurs as erythrocytes infected with trophozoites and schizonts of P. Falciparum adhere to each other, to uninflected erythrocytes and to specific receptors of blood capillaries.
• This causes capillary blockage with hemorrhages
  Vascular obstruction of the small blood vessels in vital organs brain, lungs, heart

Question 23

Describe cerebral malaria

Answer 23

In p. falciparum
- patient presents with loss of consciousness, rapid progression to coma

Question 24

Describe gastrointestinal disturbances in malignant malaria

Answer 24

Dysentery and profuse diarrhea in severe cases

Question 25

Describe Black water fever (cause, symptoms)

Answer 25

1) May result from:
- repeated p.falciparum attacks
-incomplete treatment

2) Autoimmune severe intravascular hemolysis of parasitized and non-parasitized RBCs may occur leading to acute tubular necrosis, hemoglobinuria, black urine and renal failure.

Question 26

Describe renal affection in malaria

Answer 26

1) In plasmodium falciparum:
- Tubular degeneration due to anoxia
- Black water fever: due to repeated attacks of p. falciparum infection and incomplete treatment.
Autoimmune severe intravascular hemolysis of parasitized and non-parasitized RBCs may occur leading to tubular necrosis, hemoglobinuria, blackish urine and renal failure.
- May be autoimmune phenomena due to development of antibodies to infected RBCs.

2) In Plasmodium malariae due to deposition of immune complexes in the glomerular tubules leading to nephrotic syndrome.

Question 27

What is relapse?

Answer 27

Relapse:
• Recurrence of symptoms and reappearance of the parasite in peripheral blood film within a few weeks to few years after apparent cure of primary infection.
-It is due to reactivation of dormant hypnozoites lying within the hepatocytes with formation of liver schizonts that rupture releasing merozoites that invade RBCs.
• It occurs in Plasmodium vivax or Plasmodium ovale infection.
• It does not occur in cases of Plasmodium falciparum or Plasmodium malaria infections as hypnozoites do not exist.

Question 28

What is Premunition/ Infection-immunity?

Answer 28

It is the resistance
to reinfection when infection causes little parasitaemia
(asymptomatic)

Question 29

What is the prepatent period?

Answer 29

It is the time elapsing between the inoculation of the sporozoite & the first appearance of the
parasite in the blood(6-9days)

Question 30

What is the incubation period?

Answer 30

It is the time elapsing between the inoculation of the sporozoite in man &the first appearance
of malarial clinical signs (malarial paroxysm) 10-15 days but
may be longer according to the species

Question 31

Describe direct methods of malaria diagnosis

Answer 31

1. Direct methods: – i. Microscopy (Gold standard of diagnosis of malaria):
   - Giemsa or Leishman stained thin and thick blood film.
   thin film - easier morphological differentiation
   thick film - easier detection of parasites due to RBC hemolysis

• In p.vivax, oval and malariae all stages can be found
• In p.falciparum only ring stage and gametocytes can be found due to RBC sequestration in blood vessels.

2) Quantitative buffy coat
- Anti-coagulated blood is centrifuged in a capillary tube coated with fluorescent dye.
- following centrifugation, malaria parasites are concentrated bellow the buffy coat layer.

3) Detection of circulating antigens (Rapid malaria diagnostic tests):
- These tests are simple, rapid, sensitive and highly specific.

4) Detection of plasmodium-specific genes by PCR

Question 32

Describe Indirect methods

Answer 32

• Detection of antibodies in serum by IHA, IFAT and ELISA; important for screening blood donors.

Question 33

How are anti-malarial drugs classified?

Answer 33

1) Schizonticidal drugs:
Acts on asexual erythrocytic stages
eg.4aminoquinolines
-Chloroquine
Pyrimethamine (Daraprim)

2) Anti relapse drugs:
Destroy exoerythrocytic forms (Hypnozoites) in liver preventing relapse in P.vivax & P.ovale eg.8 aminoquinolines (Primaquine, Pamaquine)

3)Gametocidal drugs
Destroy gametocytes
aminoquinolines Gametostatic drugs which prevent complete development of gametocytes in mosquitoes
eg.Proguanil.

Question 34

How is malaria treated?

Answer 34

General approach to treatment:
a. General measures: bed rest, cold sponging, antipyretics and sedatives for headache, regulation of fluid intake and electrolytes balance.
b. Treatment regimen: Malaria treatment should:
-destroy asexual blood forms to cure the clinical attacks
-destroy exo-erythrocytic forms to prevent relapse
-destroy gametocytes to prevent transmission. No single drug is useful but a combination of
drugs.
 Treatment of relapsing malaria (vivax and ovale malaria):
I. Chloroquine (blood schizonticide).
II. Primaquine (anti-relapse tissue schizonticide) for radical cure and elimination of gametocytes.
 Treatment of non-relapsing malaria (falciparum, quartan and transfusion
malaria of any species):
i. Chloroquine
ii. In severe acute attacks with vomiting or cerebral complications it is given by intravenous infusion until oral therapy is possible.
 Treatment of resistant falciparum malaria (Chloroquine-resistant):
i. Combination therapy as Fansidar (Pyrimethamine-Sulfadoxine), Fansimef
(Pyrimethamine-Sulfadoxine-Mefloquine) & artemisinin based combination therapy
 Black Water fever: Chloroquine or Pyrimethamine (Quinine and Primaquine are contra-indicated because they precipitate haemolysis

Question 35

What are some of the priority measures againts malaria?

Answer 35

*Early diagnosis and treatment, especially for young children
and pregnant women
*Indoor insecticide spraying
*Distribution of insecticide-treated mosquito nets
*Household sanitation and clearing mosquito breeding sites
*Coordination between health and other services
*Screening of blood donors.
*Use of disposable syringes.
*Production of vaccines that prevent infection, or minimize
the symptoms or stop transmission (trials).

Question 36

What are some anti-mosquito measures?

Answer 36

• Using insecticide sprays in homes and outbuildings
• Placing screens on doors and windows
• Using permethrin-impregnated mosquito netting over beds
• Applying mosquito repellents containing DEET on exposed areas of the skin.
• Wearing long pants and long-sleeved shirts, particularly between dusk and dawn, to protect against mosquito bites
• If mosquito exposure is likely to be long or involve many mosquitoes, spraying permethrin on clothing before it is worn

Question 37

can rbcs be infected by multiple parasites?

Answer 37

• RBCs can be infected with
  multiple organisms at the same time. Up to 12 parasites may infect a single RBC
• Plasmodium has up to 3
  parasites/RBC

Question 38

what are the subfamilies of mosquitoes?

Answer 38

Subfamily Culicine:
Culex, Aedes,
Mansonia,…etc.

Subfamily Anophelinae:
Anophele

Question 39

what type of life cycle do mosquitoes have?

Answer 39

complete metamorphosis

Question 40

what is the distribution of mosquitoes?

Answer 40

Cosmopolitan

Question 41

Define bionomics

Answer 41

Bionomics means the habits of different stages

Question 42

Describe the adult stage of the mosquito life cycle

Answer 42

Mosquitoes breed in water collections and rice fields

• Both sexes feed on plant nectar as source of sugar to
  get energy

*ONLY females bite to obtain blood-meals necessary
for egg development.

• They secrete saliva containing ANTICOAGULANTS;
  this causes hypersensitivity and prevents coagulation of blood of the host.
• Female mosquitoes differ in type of blood they prefer,
  those who prefer human blood are called anthropophilic while those preferring animal blood are called zoophilic.

UNIT II: Red Blood Corpuscles (RBCs) (Erythrocytes).
Anopheles gambiae is the most efficient malignant malaria vector. Anopheles pharoensis and Anopheles sergenti are the chief vectors of human malaria in Egypt.

Question 43

do mosquitoes hibernate?

Answer 43

*In winter they hibernate in dark cervices.

Question 44

how are mosquitoes a causative agent of disease?

Answer 44

Biting nuisance and allergic dermatitis:
Mosquitoes cause an allergic dermatitis due to the bite and the injection of foreign protein appears as red irritating swellings.

Question 45

how do mosquitoes act as a vector of pathogens? (parasitic)

Answer 45

• Parasitic diseases
  a-Protozoal disease (Human malaria):
• Transmitted by the bite of infected female ANOPHELES
  (DH)
  *Mode of transmission: cyclopropagative transmission.
  *Mode of infection: Inoculation of infective stage of Plasmodium spp. (sporozoites) during biting.

Question 46

how do mosquitoes act as a vector of pathogens? (filariasis, MOI, MOT)

Answer 46

Helminthic diseases (FILARIASIS):
¡- Bancroftian filariasis caused by Wuchereria bancrofti and transmitted by Culex.

il- Brugian filariasis caused by Brugia malayi and transmitted by
Mansonia and Anopheles.

Mode of transmission- cyclodevelopmental

• Mode of infection: Third stage filariform larva pierces the Dutton’s membrane, and pierces skin by its own activity.

Question 47

Diseases transmitted by mosquitoes (arbovirus)

Answer 47

A) Yellow fever
B) Dengue fever
C) Rift Valley Fever
D) West Nile virus Encephalitis

Question 48

Describe the physical control of mosquitoes

Answer 48

By modifying the natural conditions to become unsuitable for breeding of the aquatic stages, by:
a. Filling in and drainage of water collections and swampy areas.
b. Increasing slopes of canals to increase water flow.

Question 49

Describe the biological control of mosquitoes

Answer 49

The methods include the use of
a. Predators: which feed on immature stages of mosquitoes. Include:
· Gambusia afinis fish, which feeds on larvae and pupae.

b. Pathogens:
The bacteria Bacillus thurnigiensis (BT-14)
· It is the most effective pathogen, acts by endotoxins as stomach poison.
*It forms spores which are highly toxic to mosquito larvae but safe for humans.

Question 50

Describe the chemical control of mosquitoes

Answer 50

a. Non-volatile oil as solar, diesel oil, or malariol.

When sprayed on water surface they form a continuous film and therefore act as respiratory poisons which suffocate and poison aquatic forms (eggs, larvae, pupae)

b. Paris green: lt is a micro-crystalline powder green in colour. It is a double salt of copper acetate & copper meta-arsenite. It is a stomach poison. It is applied to be spread as fine dust on the surface of water killing surface feeders such as Anopheline larvae when ingested
It does not kill the pupa because it is a non feeding stage.

c. Residual insecticides: These are stomach and cuticle poisons that kill larvae and pupae. Temephos is an organophosphorus compound of lower toxicity to humans.

d. Insect growth regulators (IGRs): These are compounds that arrest larval development of insects (methoprene) or inhibit chitin formation in the immature stages.

Question 51

Describe mosquito control directed at adults

Answer 51

1. Personal protection:
   - a. Screening windows and doors of houses by wire screens.
   - b. Sleeping under mosquito nets in endemic area.
   ~ c. Using repellents
2. Indoors or outdoors spraying of insecticides
   a. Non-residual insecticides as Pyrethrum a plant extract which is a cuticle poison used as aerosol.
   b. Residual insecticides that have a long-lasting effect for months as:
   - i. Organo-phosphorous compounds e.g., Malathion and Dipterex.
   -‘i. Carbamates e.g., Sevin and Baygon.
3. Using light traps usually give good results.
4. Using animal barriers (zooprophylaxis) to deviate mosquitoes from feeding on man.
5. Sterilization of male mosquitoes: either chemically or by irradiation or by using genetic engineering techniques to produce infertile female.

Question 52

Indoors or outdoors spraying of insecticides

Answer 52

a) Non-residual insecticides such as Pyrethrum: plant extract which is a cuticle poison used as aerosol

b. Residual insecticides that have a long-lasting effect for months:
- organo-phosphorous compounds
-carbamates

Question 53

What are the 2 subspecies of African trypanosomes?

Answer 53

Trypanosoma b.gambiense - (causing West African or Gambian trypanosomiasis)

Trypanosoma b. rhodesiense (causing East African or Rhodesian trypanosomiasis)

Question 54

Describe the morphology of the African trypanosomiasis vector

Answer 54

Two morphological forms are found:

1) Trypomastigote in vertebrate host: Exists in 3 forms:
- Long slender form (30 micrometers)
-Short stumpy form (15 micrometers)
-Intermediate form (20 micrometers)

2) Epimastigote in vector and culture media

Question 55

Describe African tryp. life cycle in vertebrate host

Answer 55

1) Infected tsetse fly injects metacyclic trypomastigotes in vertebrate host when taking a blood meal

2) The parasites enter the lymphatic system and pass into the bloodstream.

3)They transform into polymorphic trypomastigotes (extracellular) which are carried to other sites

Question 56

Describe life cycle of African tryp in vector

Answer 56

1) when a tsetse fly bites an infected host, it ingests polymorphic trypomastigotes which multiply in its midgut

2) The trypomastigotes pass forward to the hypopharynx where they change to epimastigotes.

3) Epimastigotes migrate to salivary glands to change to the metacyclic trypomastigotes, thus the tsetse fly becomes infective

4) Parasites develop in the anterior part of the digestive tract of Glossina spp.

Question 57

what are the hosts of African trypanosomiasis?

Answer 57

Vertebrate host: Man and RH
Reservoir hosts:
- Man is the main reservoir for T. gambiense
-Wild game animals and domestic animals are reservoir hosts for T. rhodesiense (mainly zoonotic)

Question 58

what is the vector for African trypanosomiasis?

Answer 58

Glossina palpalis for Trypanosoma gambiense

Glossina morsitans for Trypanosoma rhodesiense

Question 59

Habitat of African Trypanoma

Answer 59

blood, lymph, tissue space of various organs and CNS

Question 60

Mode of infection and IS of African Trypanosomoiasis

Answer 60

1) Through the bite of glossina injecting metacyclic trypomastigotes (infective stage)

2) Blood borne (contaminated needles)

3) Congenital transmission

Question 61

Explain the antigenic variation of African Trypanosomes

Answer 61

• Virulence of African Trypanosomes is attributed to their ability to change the surface coat of the trypomastigote, helping evade the host humoral immune response
  — The trypomastigote is covered with a glycoprotein layer called variable Surface glycoprotein.
  – This protein is changed every 5-7 days
  –This change is responsible for successive waves of parasitemia every 7-14 days

Question 62

Pathogenesis of African tryp.

Answer 62

TA gambiense:
- long duration
- mild
-chronic
- ends fatally with CNS involvement after several years

TA rhodesiense:
- acute
- short course
- ends fatally within a year

-

Question 63

clinical manifestations of African tryp.

Answer 63

1) Trypanosomal chancre
2) Stage 1 - haemolymphatic stage
3) Meningoencephalitic stage

Question 64

what is trypanosomal chancre?

Answer 64

-Local inflammatory reaction at the site of the bite.
-Appears as red nodule (3-4cm) 1-3 weeks after the bite
-It resolves spontaneously with no scars
- Appears more in T.rhodesiense infection

Question 65

Describe stage 1 of African tryp. clinical manifestations (hemolymphatic stage)

Answer 65

1)The parasites spread through the blood and lymph

2) toxic allergic manifestations (intermittent fever, headache, malaise, muscle and joint pain, pruritus and a regular erythematous rash.

3) Generalized lymphadenopathy, especially in Gambian trypanosomiasis -Enlarged lymph nodes are soft and non-tender. Although any lymph node may be affected, posterior cervical regions are most frequently involved (Winterbottom’s sign)

4) Hepatosplenomegaly

5) Affection of bone marrow causes anemia, leukopenia and thrombocytopenia

6) Kerandel’s sign (delayed sensation to pain)

Question 66

Describe stage 2 of African tryp. clinical manifestations (haemolymphatic stage)

Answer 66

1) Trypomastigotes cross blood-brain barrier with perivascular cellular infiltration and petechial hemorrhages

2) Disease manifestations include:
- headache, confusion
- motor changes (slurred speech, poor coordination)
- personality changes, sensory disturbances
- Disturbance of sleep cycle with apathy, loss of consciousness, coma and death

3) patients usually present with multi-organ or cardiac failure

Question 67

Describe West African Trypanosomiasis (parasite, vector, primary reservoirs, illness, duration of illness, lymphadenopathy prominence, CNS involvement, parasitemia, epidemiology)

Answer 67

1) Trypanosoma gambiense
2) Glossina palpalis
3) Humans
4) Chronic
5) Months to years
6) Prominent
7) Late CNS disease
8) low
9) rural populations

Question 68

Describe East African Trypanosomiasis (parasite, vector, primary reservoirs, illness, duration of illness, lymphadenopathy prominence, CNS involvement, parasitemia, epidemiology)

Answer 68

1) Trypanosoma rhodesiense
2) Glossina morsitans
3) Wild game animals
4) -Acute and rapidly progressive
- Febrile paroxysms are more frequent
- Myocarditis is more common and death may occur due to congestive heart failure
5) Less than 9 months
6) Minimal
7) Early CNS involvement
8) High
9) workers in wild areas (occupational hazard) and tourists in wild parks

Question 69

Clinical diagnosis of African Tryp.

Answer 69

1) History whether patient has lived in or visited an endemic area
2) Clinical manifestations

Question 70

Direct Laboratory diagnosis of African Tryp.

Answer 70

1) Microscopy:
- Giemsa-stained blood film for detection of trypomastigote form is the most common method
- Blood concentration techniques for T. gambiense
- Microscopic examination aspirate from lymph nodes, chancre and CSF for presence of trypanosomes

Question 71

Indirect methods of African tryp. diagnosis

Answer 71

Trypanosome-specific antibodies are detected by:

1) The CATT (CARD AGGLUTINATION TRYPANOSOMIASIS TEST)
- for t. gambiense. This test is applied for screening of the population at risk in t.gambiense endemic areas.

2) ELISA or IFA test
Detection of increased immunoglobulin levels, especially IgM in blood and CSF due to antigenic variation

Question 72

Lumbar puncture and CSF examination in African tryp.

Answer 72

It is mandatory and should be performed for disease staging to determine the therapeutic choice

CSF findings in late stages include:
a. Polymorphic trypomastigotes
b. Increased lymphocyte count
c. Increased protein levels
d. Elevated IgM levels
e. Morula cells: altered plasma cells with vacuolated cytoplasm. These are invading cells for the production of IgM locally in the CNS, they are pathognomonic of HAT

Question 73

Treatment of early stage African tryp. (no CNS involvement)

Answer 73

1) Pentamidine for T. gambiense

2) Suramin for T. rhodesiense

Question 74

Treatment of late stage African tryp. (CNS involvement)

Answer 74

1) Melarsoprol (an organic arsenical compound)

2) Eflornithine (DFMO)

Question 75

Prevention and control of African Trypanosomiasis

Answer 75

A) Personal protection
- Avoid tsetse fly by Permethrin- impregnated clothing, use of DEET repellent, bed netting and screens
B) Vector control
Case detection by regular population screening programs

Question 76

Describe tsetse fly (geographical distribution, morphology, life cycle, bionomics, medical importance)

Answer 76

1) Tropical Africa
2) large insect measuring 8-17 mm
3) Complete metamorphosis
Egg - larva - pupa - adult
4) Feed on blood of vertebrates
- daytime feeder
- both sexes feed on blood
- G.morsitans is the most important vector in East Central Africa and is found in the savanna
- G. palpalis is the most important vector in West Africa and is found in gallery forests along rivers and lakes
5) As a vector transmitting sleeping sickness

Question 77

Control of tsetse fly

Answer 77

1) cleaning of riverine vegetations for G.palpalis while spraying insecticides on forests and elimination of reservoir animals for G. mositans
2) Use of insecticides (DDT) and use of fly traps
3) Release of infertile males: males are reared and irradiated with gamma rays before release in the wild

Question 78

Morphological forms of Trypanosoma cruzi (American)

Answer 78

• In vertebrate hosts:

1. Trypomastigote form in circulating blood: monomorphic, Slender C or U shaped (20 um).
2. Amastigote form intracellularly mainly in cardiac muscles: Round or oval forms (2-6 um).

> In vector:
3. Epimastigote form:
Spindle shape, found in vector (hindgut) & culture.

Question 79

Life cycle of trypanosoma cruzi in vertebrate host

Answer 79

1. Infected reduviid bug (Triatoma megista) releases metacyclic trypomastigotes (infective stage)
   in its feces at the site of the bite wound of the host when taking a blood meal.
   -Trypomastigotes enter through the wound or through intact mucosal membranes, such as the conjunctiva.
2. Inside the host, the trypomastigotes invade cells, where they differentiate into intracellular amastigotes.
3. Amastigotes undergo asexual reproduction and differentiate into trypomastigotes, then released to the bloodstream.

N.B: The bloodstream trypomastigotes do not replicate. Replication resumes only when the parasites enter cells in its amastigote form.

Question 80

Life cycle of trypanosoma cruzi in vector

Answer 80

1. Trypomastigotes are ingested by the reduviid bug when they take blood meal from an infected mammalian host. The ingested trypomastigotes transform into epimastigotes in the vector’s midgut, and finally differentiate into infective metacyclic trypomastigotes in the hindgut (posterior station development).
2. Metacyclic trypomastigotes are excreted from insects with the feces and infect new hosts through the skin or mucous membranes i.e., mode of infection is contaminative in type (Stercoraria).
3. Transmission of monomorphic trypanosomes in reduviid
   bug is cyclopropagative (the parasite changes in shape (morphology) and increase in number.

Question 81

Vertebrate host of trypanosoma cruzi

Answer 81

Man and RH

Question 82

RH of American trypanosoma

Answer 82

Dogs, cats, armadillos and rodents

Question 83

Vector of American Trypanosoma

Answer 83

Reduviid bug (Triatoma megista)

Question 84

Habitat of American Trypanosoma

Answer 84

Habitat: Amastigote are intracellular forms present mainly in tissues of mesenchymal origin as heart muscle, smooth muscles, brain and macrophage-phagocyte (reticuloendothelial) system and Monomorphic Trypomastigote form are extracellular forms present in the blood.

Question 85

Mode of Infection and IS of American trypanosoma

Answer 85

1. Mainly by contamination of bite wound by triatomine bug feces containing metacyclic trypomastigotes (infective stage); after they bite and ingest blood, they defecate at the site of bite. When the human or animal host scratches the bite area or intact mucous membranes, penetration of the infected feces is facilitated. It is a vector-bore disease.
2. Blood transfusion.
3. Congenital transmission
4. Organ, tissue or cell transplanted from an infected donor.

Question 86

Epidemiology of American Tryp.

Answer 86

• Chagas’ disease is a zoonosis occurring throughout Latin America and affecting estimated 12-19 million people. It is a leading cause of cardiac disease.
• Reduviid (triatomine) bugs live in close association with reservoir hosts (e.g. dogs, cats, armadillos).
• The large reservoir of T. cruzi parasites in wild animals of the Americas means that the parasite cannot be eradicated. The control targets are elimination of the transmission and health education.

Question 87

Describe Acute stage of Chagas’ disease

Answer 87

Acute Chagas disease occurs mainly in infants and children. It occurs immediately after infection (I.P: 1-2 weeks), may last up to a few weeks or months (1-4 months).

1) At the site of infection, a skin lesion (Chagoma) in the form of erythematous indurated area, or a purplish swelling of the lids of one eye (Romana’s sign) occurs where the parasite entered into the skin or mucous membrane

2) Organisms rapidly spread to lymph nodes, blood & to other organs cause generalized manifestations as fever, headache, malaise, lymphadenopathy & mild hepatosplenomegaly.

3) Most acute cases resolve over a period of a few weeks or months, or pass to chronic stage. Death may occur due to severe myocarditis or meningoencephalitis.

Question 88

Describe Chronic stage of American Tryp

Answer 88

The clinical manifestations of chronic Chagas’ disease depend on localization of parasite. For example, intracellular amastigotes destroy the intramural neurons of the autonomic nervous system in the intestine and heart.

The most serious manifestations include:
1. Chagas’ cardiomyopathy:
arrhythmias, Conduction defects,
dilated cardiomyopathy & congestive heart failure.

II. Chagas’ digestive disease: Damage of the Gl system and disturbances of peristalsis lead to dilatation with megaesophagus and megacolon, and weight loss, difficulty in swallowing, regurgitation & chronic constipation.

Question 89

Clinical diagnosis of American Tryp

Answer 89

1. History whether patient has lived in or visited endemic areas.
2. Clinical signs and symptoms

Question 90

Direct methods of Laboratory diagnosis of American Tryp

Answer 90

1. Microscopy:
   Giemsa stained thin and thick blood smears: direct blood film or concentration techniques, such as buffy coat technique. Trypomastigotes may be easily detected in blood during acute stages in young children, however, in chronic disease, this stage is rare or absent.
   Diagnostic stage: Trypomastigote form (monomorphic).

Histopathological examination of lymph node and skeletal muscle, biopsy might reveal intracellular amastigotes.
Diagnostic stage: amastigote form.

Culture: show epimastigote form

ili. Animal inoculation:
Inoculation into mice.

iv. Xenodiagnosis
• It is an efficient method to demonstrate low level of parasites in blood in chronic infections.
• A Laboratory bred winged bug is starved for 2 weeks then fed on suspected patient’s blood for 3 consecutive days, 30 days later, faces and gut are examined for trypomastigotes.

Question 91

Indirect methods of American Tryp diagnosis

Answer 91

2. Indirect methods:
   Serological tests include: IA, IHA, ELISA & CF tests.
3. Polymerase chain reaction (PCR).
   c. Imaging: Chest x-ray
   - Echocardiogram
   - Electrocardiogram (ECG).

Question 92

Treatment of American Trypanosomiasis

Answer 92

Treatment:
• No medications are given to patients with the chronic phase. Chronic-phase patients are usually treated using treatments directed at the specific symptoms or organ damage.
• The two drugs used for treatment of Chagas’ disease are Benznidazole and Nifurtimox. Both medicines are almost 100% effective in curing the disease if given soon after infection at the onset of the acute phase.

Question 93

Prevention and control of American Tryp in endemic areas

Answer 93

Prevention and control:
A. Endemic areas
1. Vector control is the most useful method to prevent Chagas’ disease.
Measures include:
House improvements to prevent vector infestation.
-Spraying of houses and surrounding areas with residual insecticides.
- Mechanical elimination of the vector.
2. Personal preventive measures such as bed nets.
3. Health education.
4. Avoid pets in the home environment.
5. Screening of blood donors.
6. Screening of newbors and other children of infected mothers to provide early diagnosis and treatment.
7. Testing of organ, tissue or cell donors.

Question 94

Prevention and control of American Tryp in non-endemic areas

Answer 94

B. Non-endemic areas
These are other regions where Chaga’s disease is found but is not endemic (e.g., US)
1. Screening of blood donors.
2. Testing of organ, tissue or cell donors.
3. Mother to -baby screening of newboms and other children of infected mother to provide early diagnosis and treatment.

Question 95

Describe Triatoma Megista (distribution, morphology, life cycle )

Answer 95

Geographical distribution: Central and South America.

Morphology:
Large insect (2-3 cm), dark brown or black-with reddish markings on thorax and abdomen.

Life cycle:
Incomplete metamorphosis:
Egg
Nymph
Adult

Question 96

Bionomics of Triatoma Megista

Answer 96

Bionomics:
• Temporary ectoparasite.
•Males, females and nymphs suck blood at night while the host is sleeping, usually on the exposed face near the nose, eyes or mouth (Kissing bug).
• The vector is reduviid (triatomine) bugs which typically live in the cracks of poorly constructed homes in rural or suburban areas.

Question 97

Medical importance of Triatoma Megista

Answer 97

Medical importance:
• As causative agent of disease:
Reduviid bites usually present as papular urticaria.
• As a vector transmitting diseases:
In rural areas of South America, they are the vectors for Trypanosoma cruzi, which causes Chagas’ disease.

Question 98

Control of Triatoma Megista

Answer 98

.
Control:
1. Screening of doors and windows and use of impregnated bed nets.
2. Eradication of reservoir hosts and use of residual insecticides as Malathion. DDT is not effective.
3. Plastering of cracks of walls and use of insecticidal.

Question 99

What is recrudescence?

Answer 99

• Recurrence of symptoms and reappearance of the parasite in peripheral blood film within few weeks to few years after apparent cure of primary infection.
-It is due to reactivation of blood stages surviving in small numbers in RBCs after primary infection. The parasites remain dormant in the RBCs (due to inadequate treatment) until the host’s immune response becomes weaker, and then they multiply to a level sufficient to cause clinical illness once more. It occurs in all species of Plasmodium.