Parasitology Flashcards
1
Q
What is a bloodborne parasite?
A
- The parasite can be found in the bloodstream of infected people
- 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).
- In nature, many bloodborne parasites are spread by insects (vectors), so they are also referred to as vectorborne diseases.
2
Q
Examples of parasitic diseases that can be bloodborne
A
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.
3
Q
What is malaria
A
-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.
4
Q
Describe Life cycle of plasmodium
A
- 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
5
Q
Where does malaria usually occur?
A
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.
6
Q
What species of plasmodium affect man?
A
- P. vivax,
- P. falciparum,
- P. malariae ,R.H. Chimpanzee
- P. ovale.
- P. knowlesi a 5th species prevalent in South
East Asia
- P. knowlesi a 5th species prevalent in South
7
Q
Habitat of plasmodium
A
Temporary in liver cells then Red blood cells (intraerythrocytic).
8
Q
Vector (DH) and IH of plasmodium
A
-Female Anopheles
mosquito (bites between dusk and dawn)
-Man
9
Q
Infective stage to man and mosquitoes
A
-Sporozoites
-Gametocytes
10
Q
Mode of infection of plasmodium
A
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.
11
Q
Describe life cycle of plasmodium –in liver cells–(Exo-erythrocytic schizogony cycle)
A
- 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
12
Q
Describe Cycle in the red cells: (Erythrocytic schizogony cycle +
Gametogony cycle)
A
- 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.
13
Q
Describe cycle of plasmodium in vector
A
- It takes place in the midgut of the female Anopheles mosquito.
- All ingested stages are digested except the gametocytes which complete the cycle.
- 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.
14
Q
How do you identify the plasmodium species?
A
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)
15
Q
Describe morphology of plasmodium vivax
A
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
16
Q
Describe plasmodium falciparum
A
-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.
17
Q
Describe Malaria
A
- 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.
18
Q
clinical incubation period (definition and time in malaria)
A
The time between the inoculation of sporozoites and first appearance of characteristic malaria paroxysm
- It takes 1-5 weeks according to the species
19
Q
Prodromal symptoms of malaria
A
Early cycles of multiplication cause headache, bone ache and irregular fever. may be misdiagnosed as influenza
20
Q
Malarial paroxysmal attacks (cause and occurrence in each species)
A
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.
21
Q
Describe the stages of a paroxysmal attack
A
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
22
Q
Describe Malignant Malaria (cause for severe infection
A
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
23
Q
Describe cerebral malaria
A
In p. falciparum
- patient presents with loss of consciousness, rapid progression to coma
24
Q
Describe gastrointestinal disturbances in malignant malaria
A
Dysentery and profuse diarrhea in severe cases
25
Describe Black water fever (cause, symptoms)
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.
26
Describe renal affection in malaria
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.
27
What is relapse?
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.
28
What is Premunition/ Infection-immunity?
It is the resistance
to reinfection when infection causes little parasitaemia
(asymptomatic)
29
What is the prepatent period?
It is the time elapsing between the inoculation of the sporozoite & the first appearance of the
parasite in the blood(6-9days)
30
What is the incubation period?
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
31
Describe direct methods of malaria diagnosis
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
32
Describe Indirect methods
* Detection of antibodies in serum by IHA, IFAT and ELISA; important for screening blood donors.
33
How are anti-malarial drugs classified?
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.
34
How is malaria treated?
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
35
What are some of the priority measures againts malaria?
*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).
36
What are some anti-mosquito measures?
* 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
37
can rbcs be infected by multiple parasites?
* 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
38
what are the subfamilies of mosquitoes?
Subfamily Culicine:
Culex, Aedes,
Mansonia,…etc.
Subfamily Anophelinae:
Anophele
39
what type of life cycle do mosquitoes have?
complete metamorphosis
40
what is the distribution of mosquitoes?
Cosmopolitan
41
Define bionomics
Bionomics means the habits of different stages
42
Describe the adult stage of the mosquito life cycle
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.
43
do mosquitoes hibernate?
*In winter they hibernate in dark cervices.
44
how are mosquitoes a causative agent of disease?
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.
45
how do mosquitoes act as a vector of pathogens? (parasitic)
- 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.
46
how do mosquitoes act as a vector of pathogens? (filariasis, MOI, MOT)
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.
47
Diseases transmitted by mosquitoes (arbovirus)
A) Yellow fever
B) Dengue fever
C) Rift Valley Fever
D) West Nile virus Encephalitis
48
Describe the physical control of mosquitoes
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.
49
Describe the biological control of mosquitoes
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.
50
Describe the chemical control of mosquitoes
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.
51
Describe mosquito control directed at adults
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.
52
Indoors or outdoors spraying of insecticides
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
53
What are the 2 subspecies of African trypanosomes?
Trypanosoma b.gambiense - (causing West African or Gambian trypanosomiasis)
Trypanosoma b. rhodesiense (causing East African or Rhodesian trypanosomiasis)
54
Describe the morphology of the African trypanosomiasis vector
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
55
Describe African tryp. life cycle in vertebrate host
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
56
Describe life cycle of African tryp in vector
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.
57
what are the hosts of African trypanosomiasis?
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)
58
what is the vector for African trypanosomiasis?
Glossina palpalis for Trypanosoma gambiense
Glossina morsitans for Trypanosoma rhodesiense
59
Habitat of African Trypanoma
blood, lymph, tissue space of various organs and CNS
60
Mode of infection and IS of African Trypanosomoiasis
1) Through the bite of glossina injecting metacyclic trypomastigotes (infective stage)
2) Blood borne (contaminated needles)
3) Congenital transmission
61
Explain the antigenic variation of African Trypanosomes
- 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
62
Pathogenesis of African tryp.
TA gambiense:
- long duration
- mild
-chronic
- ends fatally with CNS involvement after several years
TA rhodesiense:
- acute
- short course
- ends fatally within a year
-
63
clinical manifestations of African tryp.
1) Trypanosomal chancre
2) Stage 1 - haemolymphatic stage
3) Meningoencephalitic stage
64
what is trypanosomal chancre?
-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
65
Describe stage 1 of African tryp. clinical manifestations (hemolymphatic stage)
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)
66
Describe stage 2 of African tryp. clinical manifestations (haemolymphatic stage)
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
67
Describe West African Trypanosomiasis (parasite, vector, primary reservoirs, illness, duration of illness, lymphadenopathy prominence, CNS involvement, parasitemia, epidemiology)
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
68
Describe East African Trypanosomiasis (parasite, vector, primary reservoirs, illness, duration of illness, lymphadenopathy prominence, CNS involvement, parasitemia, epidemiology)
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
69
Clinical diagnosis of African Tryp.
1) History whether patient has lived in or visited an endemic area
2) Clinical manifestations
70
Direct Laboratory diagnosis of African Tryp.
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
71
Indirect methods of African tryp. diagnosis
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
72
Lumbar puncture and CSF examination in African tryp.
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
73
Treatment of early stage African tryp. (no CNS involvement)
1) Pentamidine for T. gambiense
2) Suramin for T. rhodesiense
74
Treatment of late stage African tryp. (CNS involvement)
1) Melarsoprol (an organic arsenical compound)
2) Eflornithine (DFMO)
75
Prevention and control of African Trypanosomiasis
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
76
Describe tsetse fly (geographical distribution, morphology, life cycle, bionomics, medical importance)
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
77
Control of tsetse fly
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
78
Morphological forms of Trypanosoma cruzi (American)
• 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.
79
Life cycle of trypanosoma cruzi in vertebrate host
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.
80
Life cycle of trypanosoma cruzi in vector
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.
81
Vertebrate host of trypanosoma cruzi
Man and RH
82
RH of American trypanosoma
Dogs, cats, armadillos and rodents
83
Vector of American Trypanosoma
Reduviid bug (Triatoma megista)
84
Habitat of American Trypanosoma
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.
85
Mode of Infection and IS of American trypanosoma
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.
86
Epidemiology of American Tryp.
• 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.
87
Describe Acute stage of Chagas’ disease
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.
88
Describe Chronic stage of American Tryp
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.
89
Clinical diagnosis of American Tryp
1. History whether patient has lived in or visited endemic areas.
2. Clinical signs and symptoms
90
Direct methods of Laboratory diagnosis of American Tryp
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.
91
Indirect methods of American Tryp diagnosis
2. Indirect methods:
Serological tests include: IA, IHA, ELISA & CF tests.
3. Polymerase chain reaction (PCR).
c. Imaging: Chest x-ray
- Echocardiogram
- Electrocardiogram (ECG).
92
Treatment of American Trypanosomiasis
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.
93
Prevention and control of American Tryp in endemic areas
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.
94
Prevention and control of American Tryp in non-endemic areas
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.
95
Describe Triatoma Megista (distribution, morphology, life cycle )
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
96
Bionomics of Triatoma Megista
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.
97
Medical importance of Triatoma Megista
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.
98
Control of Triatoma Megista
.
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.
99
What is recrudescence?
• 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.
