Blood and Tissue Protozoal Infections
Session 37: Blood and Tissue Protozoal Infections
Total Session Time: 120 minutes
Pre-requisites
Students Learning Tasks
By the end of this session students are expected to be able to:
Malaria, Toxoplamosis andTrypanosomiasis
Resources Needed:
SESSION OVERVIEW
|Step |Time |Activity/ |Content |
| | |Method | |
|1 |5 minutes |Presentation |Introduction, Learning Tasks |
|2 | |Small group |Malaria |
| |40 minutes |discussion/ | |
| | |Presentation | |
|3 | 35 |Presentation |Toxoplasmosis |
| |minutes | | |
|4 |30 minutes |Presentation |African Trypanosomiasis |
|5 |5 minutes |Presentation |Key Points |
| 6|5 minutes |Presentation |Evaluation |
SESSION CONTENTS
STEP 1: Presentation of Session Title and Learning Tasks (5 minutes)
READ or ASK students to read the learning tasks and clarify
ASK students if they have any questions before continuing
STEP 2: Malaria (40 minutes)
Cause and Transmission
various species of Plasmodium
o Plasmodium falciparum
o Plasmodium vivax
o Plasmodium ovale
o Plasmodium malariae
o Plasmodium knowlesi
mosquito.
o The malaria parasite life cycle involves two hosts.
o During a blood meal, a malaria-infected female Anopheles mosquito
inoculates sporozoites into the human host
o Sporozoites infect liver cells and mature into schizonts, which
rupture and release (merozoites (In P. vivax and P. ovale a dormant
stage (hypnozoites) can persist in the liver and cause relapses by
invading the bloodstream weeks, or even years later.)
o After this initial replication in the liver (exo-erythrocytic
schizogony), the parasites undergo asexual multiplication in the
erythrocytes (erythrocytic schizogony).
o Merozoites infect red blood cells.
o The ring stage trophozoites mature into schizonts, which rupture
releasing merozoites
o Some parasites differentiate into sexual erythrocytic stages
(gametocytes)
o Blood stage parasites are responsible for the clinical
manifestations of the disease. The gametocytes, male
(microgametocytes) and female (macrogametocytes), are ingested by an
Anopheles mosquito during a blood meal
o The parasites’ multiplication in the mosquito is known as the
sporogonic cycle
o While in the mosquito’s stomach, the microgametes penetrate the
macrogametes generating zygotes
o The zygotes in turn become motile and elongated (ookinetes) which
invade the midgut wall of the mosquito where they develop into
oocysts
o The oocysts grow, rupture, and release sporozoites, which make their
way to the mosquito’s salivary glands. Inoculation of the
sporozoites into a new human host perpetuates the malaria life
cycle.
[pic]
o The disease presentation will vary according to patient’s state of
immunity, the intensity of the infection and the presence of
accompany conditions such as malnutrition, anaemia and other
diseases.
without signs of severity or evidence (clinical or
laboratory) of vital organ dysfunction.
are no signs to indicate severe infection or dysfunction of
the vital organs.
if the host has poor or no immunity.
severity of vial organ dysfunction. Severe Plasmodium
falciparum malaria is a medical emergency.
signs of vital organ dysfunction
may lead to serious complications and even death
Signs and Symptoms
o Fever, headache, nausea, vomiting,
o Malaise, fatigue, muscle pain,
o Anorexia, chill, rigors, sweats, cough and diarrhea
o Fever and chills
o Impaired consciousness
o Change in behavior
o Prostration/extreme weakness
o Respiratory distress
o Circulatory collapse/shock
o Vomiting everything
o Multiple convulsions
o Deep breathing and respiratory distress
o Abnormal bleeding and signs of anemia
o Clinical jaundice and evidence of vital organ dysfunction
o Severe malaria can be fatal without treatment
o Inability to drink or breastfeed
o Complications of severe malaria include;
acidosis, acute renal failure or pulmonary oedema
o In Tanzania the commonest presentations of severe malaria are;
Treatment and Prevention
o Artemisinin-based combination therapy (ACT) is recommended by the
WHO to treat uncomplicated malaria.
o ACT is artemisinin combined with a partner drug. The role of
artemisinin is to reduce the number of parasites within the first 3
days of infection, while the partner drugs eliminate the rest.
o These drugs include;
managed by quinine tablet
o Hypoglycaemia is the major problem in the management of severe
malaria especially in young children and pregnant women.
Hypoglycaemia should be looked and treated accordingly. Other
features like anaemia should also be addressed
|Activity: Take home Assignment (10 minutes) |
| |
|DIVIDE students in groups or individual. |
| |
|ASK the students to work on the following assignment |
| |
|Explain the dose and dosing schedule for antimalarial drugs used in |
|the treatment of uncomplicated and severe malaria in Tanzania |
| |
|ALLOCATE time for students to do the assignment and submit |
| |
|REFER students to recommended references |
|Activity: Buzzing (5 minutes) |
| |
|ASK students to pair up and buzz on the following question for 2 |
|minutes |
| |
|How is malaria prevented? |
| |
|ALLOW few pairs to respond and let other pairs to add on points |
|not mentioned |
| |
|WRITE their response on the flip chart/board |
| |
|CLARIFY and SUMMARIZE by using the content below |
o Clearing of bushes around houses to destroy mosquito breeding sites
o Sleeping under insecticide-treated mosquito nets to avoid bites when
sleeping
o Using mosquito repellents
o Prevention of malaria in pregnancy (Intermittent preventive
treatment in pregnancy (IPTp))
malaria from pregnant women to the foetus
gestational age and the second IPTp dose at 28 – 32 weeks
STEP 3: Toxoplasmosis (35 minutes)
Cause and Transmission
Toxoplama gondii. Toxoplasmosis is a disease of blood and lymphatic
system
to cause disease in them.
family Felidae (domestic cats and their relatives
o Consumption of undercooked contaminated meat of animals harboring
tissue cysts
o Consuming food or water contaminated with cat feces
o Exposure to contaminated environmental samples (such as fecal-
contaminated soil or changing the litter box of a pet cat)
o Blood transfusion or organ transplantation
o Transplacentally from mother to fetus
earlier in pregnancy the transmission occurs. Potential results
can be
enlargement or smallness of the head)
o Unsporulated oocysts are shed in the cat’s feces
o Oocysts take 1-5 days to sporulate in the environment and become
infective.
o Intermediate hosts in nature (including birds and rodents) become
infected after ingesting soil, water or plant material contaminated
with oocysts
o Oocysts transform into tachyzoites shortly after ingestion.
o These tachyzoites localize in neural and muscle tissue and develop
into tissue cyst bradyzoites
o Cats become infected after consuming intermediate hosts harboring
tissue cysts or directly by ingestion of sporulated oocysts
o Animals bred for human consumption and wild game may also become
infected with tissue cysts after ingestion of sporulated oocysts in
the environment
o In the human host, the parasites form tissue cysts, most commonly in
skeletal muscle, myocardium, brain, and eyes; these cysts may remain
throughout the life of the host
[pic]
Signs and Symptoms
o Body aches
o Swollen lymph nodes
o Headache
o Fever
o Fatigue
may develop;
o Headache
o Confusion
o Poor coordination
o Seizures
o Lung problems that may resemble tuberculosis or Pneumocystis
jiroveci pneumonia, a common opportunistic infection that occurs in
people with AIDS
o Blurred vision caused by severe inflammation of your retina (ocular
toxoplasmosis)
Treatment and Prevention
o Sulphadiazine
o Pyrimethamine
o Folic acid
o Clindamycin
o Personal hygiene e.g. washing hands after contact with cat
o Avoiding exposure to cat faeces
STEP 4: African Trypanosomiasis (30 minutes)
Cause and Transmission
microscopic parasites (Trypanosmes) of the Trypanosoma brucei complex
belonging to the genus Trypanosomes in the family Trypanosomatidae.
mammalian host) and require an intermediate (insect) host (usually an
insect) to complete their life cycle
o Trypanosome undergoes complex changes during its life cycle to
facilitate survival in the insect gut and the mammalia bloodstream.
humans
species can also be found in animals. Wild game animals and cattle are
the main reservoir of T. b. rhodesiense.
o Other modes of transmission are possible.
o T.b. gambense is found in Central and Western Africa
months or years before symptoms emerge
o T.b. rhodesiense is found in Southern and Eastern Africa
faster developing
o During a blood meal on the mammalian host, an infected tsetse fly
(genus Glossina) injects metacyclic trypomastigotes into skin
tissue.
o The parasites enter the lymphatic system and pass into the
bloodstream.
o Inside the host, they transform into bloodstream trypomastigotes,
are carried to other sites throughout the body, reach other blood
fluids (e.g. lymph, spinal fluid), and continue the replication by
binary fission
o The entire life cycle of African Trypanosomes is represented by
extracellular stages.
o The tsetse fly becomes infected with bloodstream trypomastigotes
when taking a blood meal on an infected mammalian host
o In the tsetse fly’s midgut, the parasites transform into procyclic
trypomastigotes, multiply by binary fission, leave the midgut, and
transform into epimastigotes
o The epimastigotes reach the fly’s salivary glands and continue
multiplication by binary fission
o The cycle in the fly takes approximately 3 weeks
[pic]
o In the first stage, the parasite is found in the peripheral
circulation, but it has not yet invaded the central nervous system.
o In the second stage, the parasite crosses the blood-brain barrier
and infects the central nervous system
of disease progression, and the clinical features depend on which form
of the parasite (T. b. rhodesiense or T. b. gambiense) is causing the
infection. However, infection with either form will eventually lead to
coma and death if not treated.
Signs and Symptoms
transmit infection), the parasite multiplies in the lymph and the blood
of the person bitten
o Headaches, fever, weakness, pain in the joints, lymphadenopathy
(Winterbottom’s sign), and stiffness.
o People who become infected may or may not show signs of illness
immediately, but over time the parasite crosses the blood-brain
barrier and migrates to the central nervous system.
Treatment
complex administration of the drugs currently available for treatment.
o Pentamidine (for T.b. gambianse)
o Suramin (T.b. rhodesiense)
o Melarsoprol
o Eflornithine
o Nifurtimox (is used in combination under special authorizations)
o Pentamidine and suramin are used in the first or early stage of
T.b.gambiense and T.b. rhodesiense infections respectively.
|Activity: Take home Assignment (10 minutes) |
| |
|DIVIDE students in groups or individual. |
| |
|ASK the students to work on the following assignment |
| |
|Prepare a presentation on the doses and dose schedules for medicines |
|used in the treatment of African trypanosomiasis in Tanzania. |
| |
|ALLOCATE time for students to do the assignment and submit |
| |
|REFER students to recommended references |
Prevention
o Protection against bites by tsetse flies
material in neutral colours that blend with the background
environment. (Tsetse flies are attracted to bright or dark
colours, and they can bite through lightweight clothing)
the motion and dust from moving vehicles.
o Case finding and early treatment
o Vector control
STEP 5: Key Points (5 minutes)
(Trypanosomes) of the Trypanosoma brucei complex that are transmitted by
Typanosoma brucei gambiense and Trypanosoma brucei rhodesiense
belonging to the genus Trypanosomes
of disease progression, and the clinical features depend on which form
of the parasite (T. b. rhodesiense or T. b. gambiense) is causing the
infection. Both infections eventually lead to coma and death if not
treated.
STEP 6: Evaluation (5 minutes)
References
Hugo and Russell (2011), Pharmaceutical Microbiology 8th Edition, Willey-
Blackwel publications
Karen C. Carroll et al (2013); Jawetz, Melnick and Adelberg’s Medical
Microbiology 26th Ed. McGraw Hill Co. Inc.
Greenwood et al (2012); Medical Microbiology, 18th edition Churchill
Livingstone
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