Malaria presentation

1. MALARIA AND
TOXOPLASMOSIS
Name: Rohan Rahul Prasad
ID: 20170123

2. MALARIA

3. TABLE OF CONTENT
1. Introduction
2. Epidemiology and Risk
Factors
3. Pathophysiology
4. Incubation period
5. Clinical presentation
6. Complications
7. Physical Examination
8. Diagnosis
9. Prevention
10. Treatment
11. Prognosis
12. Conclusion
13. References

4. INTRODUCTION
• Malaria is a potentially life threatening disease caused
by infection with Plasmodium protozoa transmitted by
an infective female Anopheles mosquito.
• Once Plasmodium enters the bloodstream, it infects
and destroys mainly Liver and Red Blood cells.
Malaria is caused by 5 species of Plasmodium:
• P. falciparum
• P. vivax pose the greatest threat
• P. ovale
• P. malariae
• P. knowlesi

5. EPIDEMIOLOGY OF MALARIA
• Malaria is a SERIOUS GLOBAL HEALTH PROBLEM.
• It is widely distributed in tropics and subtropics of
Africa, Asia and Latin America.
• Malaria affecting 300-500 million people
annually.
• Malaria causing 1-3 million deaths each year.
• In 2017 – Estimated 219 million cases of malaria
in 87 countries. Number of deaths stood at
435000.

7. SOUTH PACIFIC

8. MALARIA AFFECTS MILLIONS !
Young Children aged 6 months to 3 years
Travelling in a region where malaria is present or
common:
• Travelling without immunity.
• Being outdoors, especially in rural areas
• Not taking steps to protect yourself from
mosquito bites.
Pregnant women
Patients with other conditions such as HIV/AIDS.

10. • Plasmodium- infected female anopheles
mosquito hunts for a blood meal in the evening
through the night.
• At this point, plasmodium is in the stage of
development called a sporozoite in the
mosquito’s salivary gland.
• Mosquito injects sporozoites during the blood
meal and spills into the bloodstream.
• Sporozoites disappear from the human blood
within half an hour and enter the liver to engage
in asexual reproduction called Schizogony.

11. NOTE !
• P. vivax and P. ovale may persist in liver cells as
dormant forms, hypnozoites, capable of developing
into merozoites months or years later. Thus the first
attack of clinical malaria may occur long after the
patient has left the endemic area, and the disease may
relapse after treatment if drugs that kill only the
erythrocytic stage of parasite are given.
• P. falciparum and P. malariae have no persistent
erythrocytic phase but recrudescence of fever may
result from multiplication of parasites in red cells which
have not been eliminated by treatment and immune
processses.

12. ERYTHROCYTIC PHASE
• After some days merozoites leave the liver and
invade red blood cells (each merozoite binds to
surface receptors and invades a RBC)
• P. falciparum – is able to infect RBCs of all ages,
resulting in high levels of parasitemia (>5% RBCs
infected)
• P. vivax and P. ovale – infects only young RBCs and
thus cause a lower level of parasitemia (usually
<2%)
• P. malariae and P. knowlesi – invades older RBCs

13. ERYTHROCYTIC PHASE
• Once inside the RBCs, the merozoites undergo
asexual replication and a series of
transformational changes.
3 stages:
• Early trophozoite or ring form
• Late trophozoite
• Schizont phase

14. STAGE 3
• The parasite grows some more by metabolizing
hemoglobin and other RBC proteins to create a
toxic pigment called hemozoin, which under a
microscope looks like a brown feces smudge on
the red blood cell, and at this point the parasite is
called a schizont.
• This is the actual replicative phase in which the
parasite undergoes mitosis and differentiates into
lots of merozoites. Rupture of schizonts releases
merozoites into the blood and causes fever.

16. • Now instead of going into the erythrocytic phase
again, some of the merozoites undergoes
gametogony where they divide and give rise to
gametocytes sausage shapes sexual forms that
can be either male or female.
• These gametocytes remain in a red blood cell and
can get sucked up by another female anopheles
mosquito that might take a blood meal from an
infected person

17. • Gametocyte reaches mosquito’s gut matures
and fuse to form a zygote this part of
plasmodium life cycle is called a sporogony
(sexual reproduction).
• The zygote develops further becomes
ookinete oocyst ruptures into
mosquito’s gut releases thousands of
sporozoites navigates their way into the
mosquito’s salivary gland in order to repeat the
cycle all over again.

18. INCUBATION PERIOD

19. CLINICAL
PRESENTATION

20. • Each plasmodium species has a typical incubation period.
Importantly, virtually all patients with malaria present with
headache.
Clinical symptoms also include the following:
• Cough
• Fatigue
• Malaise
• Shaking chills
• Arthralgia
• Myalgia
Paroxysm of fever, shaking chills and sweats (every 48-72 hrs,
depending on species)

21. • The release of TNF alpha and other inflammatory
cytokines causes fever that typically occurs in
paroxysms or short bursts and corresponds to the
rupture of infected red blood cells which happens in
waves of reproductive cycles unique for each
plasmodium species.
• The classic paroxysm begins with a period of shivering
and chills, which lasts for approximately 1-2 hrs and is
followed by a high fever. Finally, the patient
experiences excessive diaphoresis, and the body
temperature drops to normal or below normal.

22. SPECIES TIME BETWEEN FEVER
PAROXYSMS
P. falciparum 36-48 hrs (variable) Malignant tertian fever
P. ovale 48 hrs Ovale tertian fever
P. vivax 48 hrs Benign tertian fever
P. knowlesi 24 hrs
P. malariae 72 hrs Quartan fever

24. Plasmodium malariae
• Usually associated with mild symptoms and
bouts of fever every third day. Parasitemia
may persist for many years with the occasional
recrudescence of fever, or without producing
any symptoms.

25. P. Ovale and P. vivax
• Illness starts with several days of continued fever
before the development of classical bouts of fever on
alternate days.
• Fever starts with a rigor. The patient feels cold and the
temperature rises to about 40 degrees Celsius.
• After half an hour to an hour the hot or flush phase
begins. It lasts several hours and gives way to profuse
perspiration and a gradual fall in temperature. The
cycle is repeated 48 hours later.
• Gradually the spleen and liver enlarge and may
become tender. Anaemia develops slowly.
• Relapses are frequent in the first 2 years after leaving
the malarious area
• Infection may be acquired from blood transfusion.

26. P. falciparum
• Most dangerous of the malarias. Patients are either
“killed” or “cured”.
• Onset is often insidious, with malaise, headache and
vomiting.
• Cough and mild diarrhea are also common
• Fever has no particular pattern
• Jaundice is common due to hemolysis and hepatic
dysfunction.
• Liver and spleen enlarge and may become tender.
• Anaemia develops rapidly, as does thrombocytopenia

27. P. falciparum CAUSES THE WORST
INFECTIONS
• Most plasmodium- infected red blood cells gets
screened and destroyed by the spleen.
• Plasmodium falciparum avoids this fate by generating a
sticky protein that coats the surface of the infected red
blood cells and these look like “knobs” or little bumps
• The protein causes the red blood cells to clump
together and clog tiny blood vessels – a process called
cytoadherence
• This blocks the flow of blood so that infected cells
aren't able to flow into the spleen, and it also blocks
blood flow from reaching other vital organs which can
wreak havoc on them.

28. • Hemolytic Anaemia + ischemic damage = Organ
failure
When the brain is affected – Cerebral malaria
• Altered mental status, seizures and coma
When liver is affected – Bilious malaria
• Diarrhea, vomiting, jaundice and liver failure
Other organs: lungs, kidney and spleen which taken
together create a sepsis like clinical picture that
can eventually lead to death.

29. OTHER COMPLICATIONS OF P.
falciparum
• Seizures – secondary to either hypoglycemia or
cerebral malaria
• Renal failure
• Hypoglycemia
• Hemoglobinuria (blackwater fever) – passage of dark
urine, described as Madeira wine colored; hemolysis,
hemoglobinemia, and hemozoinuria cause the
condition.
• Pulmonary edema
• Lactic acidosis – occurs when microvasculature
becomes clogged with P. flaciparum.
• Hemolysis resulting in severe anaemia and jaundice.
• Bleeding (coagulopathy)

30. NOTE !
• The parasites derive their energy solely from
glucose, and they metabolize it 70 times faster
than the RBCs they inhibit, thereby causing
hypoglycemia and lactic acidosis.
• The plasmodia also causes lysis of infected and
uninfected RBCs, suppression of hematopoiesis,
and the increased clearance of RBCs by the
spleen, which leads to anemia as well as
splenomegaly.
• Overtime, malaria may also cause
thrombocytopenia.

31. • Malaria may be devastating during pregnancy to
the mother and the fetus. P. falciparum is the
primary species responsible for increased
morbidity and mortality in pregnancy.
• Maternal complications are mediated by
pregnancy associated decreases in immune
function, as well as by placental sequestration of
P. falciparum parasites.
• Anemia from malaria can be more severe in
pregnant women. Fetal complications include
premature birth, anemia, low birth weight and
death.
• Malaria during the first trimester of pregnancy
increases the risk for miscarriage.

32. PHYSICAL EXAMINATION
Appearance of the patient – may be ill looking, shivering
and/or sweating. After the fever episodes, patient
appear extremely tired and sleepy. In more severe
cases of the disease, the patient may appear anemic,
with jaundice or even in coma
VITALS
Temperature – fever is often present
Pulse – tachycardia may be present
Blood pressure – hypotension (in severe cases of disease)
Respiratory rate – tachypnea may be present

33. Skin
• Cyanosis (in severe cases of disease, where there may be
respiratory distress)
• Jaundice (in severe anemia)
• Pallor may be present
• Petechiae (when there is thrombocytopenia)
Eyes
• Icteric sclera (in severe anaemia with jaundice)
• Conjunctivae may be pale
Nose
• Alar flare (in respiratory distress)
Lungs
• Pulmonary edema may be present
• Consolidation may be present with reduced breath sounds
auscultated (rarely)
• Intercostal retraction (in respiratory distress)

34. Abdomen
• Abdominal distension may be present
• Hepatomegaly
• Splenomegaly
Genitourinary
• Hematuria (in severe hemolysis)
Extremities
• Cyanosis (in severe anaemia)
• Edema (in renal failure)
Neurologic
• Coma may be present (cerebral malaria)
• Mental status may be altered
• Convulsion may occur

35. DIAGNOSIS

36. HISTORY
• Patients with suspected malaria – obtain
history of recent or remote travel to an
endemic area.
• Traveled to a tropical area at anytime in their
life.
• Determine patients immune status, age, and
pregnancy status; allergies or other medical
conditions that he or she may have; and
medications that he or she may be using.

37. • Blood culture
• Hemoglobin
concentration
• Platelet count
• Liver function
• Renal function
• Electrolyte
concentration
(especially
sodium)
• Urine analysis

38. n
• Monitoring of parameters
suggestive of hemolysis
(haptoglobin, LDH,
reticulocyte count)
• In select cases, rapid HIV
testing
• If patient is to be treated
with primaquine, G6PD
level
• If patient has cerebral
malaria, glucose level to
rule out hypoglycemia
• Chest radiograph – if
respiratory symptoms
present
• CT scan of the head – if
CNS symptoms present
• Microhematocrit
centrifugation
• Fluorescent/ultraviolet
indicator tests
• Thin and thick blood
smears
• Alternatives to blood
smear testing: rapid
diagnostic test, PCR assay
and nuclei acid sequence
based amplification.

39. APPROACH CONSIDERATIONS
• In returning travelers from endemic areas. Malaria is
suggested by triad of thrombocytopenia, elevated
lactate dehydrogenase levels and atypical lymphocytes.
• Generally, blood cultures should be drawn in a febrile
patient.
• Assess hemoglobin (decreased in 25% of patients),
platelet count (thrombocytopenia in 50-68% of
patients), and liver function
• Also monitor renal function, electrolytes (especially
sodium) and parameters suggestive of hemolysis
(haptoglobin, LDH, reticulocyte count). HIV testing may
also be indicated in select cases.

40. • If the patient is to be treated with primaquine, a
G-6-PD level should be obtained because
primaquine can result in severe hemolysis in
these patients.
• If the patient has cerebral malaria, obtain a blood
glucose level to rule out hypoglycemia as a cause
of mental-status changes. Note that intravenous
(IV) quinine can induce hypoglycemia; therefore,
blood glucose should be monitored when IV
quinine is used

41. Blood Smears
• Thick and thin films should be routinely used for
malaria diagnosis; thick films should be stained with
Giemsa or Field stain, thin films with Giemsa or
Leishman stain
• Thick smears - Three thick and thin smears 12-24 hours
apart should be obtained. The highest yield of
peripheral parasites occurs during or soon after a fever
spike; however, smears should not be delayed while
awaiting fever spikes. Thick smears are 20 times more
sensitive than thin smears, but speciation may be more
difficult. The parasitemia can be calculated based on
the number of infected RBCs. This is a quantitative test
• Thin smears - Thin smears are less sensitive than thick
smears, but they allow identification of the different
species. This should be considered a qualitative test.

43. Alternative Blood Smear Testing
Rapid Diagnostic Test (RDT)
• Immunochromatographic tests based on antibody to
histidine-rich protein-2 (PfHRP2), parasite LDH (pLDH), or
Plasmodium aldolase appear to be very sensitive and
specific.
• May be able to detect P falciparum in parasitemias that are
below the threshold of reliable microscopic species
identification
Other tests:
• PCR assay testing and nucleic acid sequence-based
amplification (NASBA), are also available for diagnosis.
• They are more sensitive than thick smears but are
expensive and unavailable in most developing countries

44. IMAGING STUDIES
• Chest radiography - if respiratory symptoms
are present.
• If CNS symptoms are present, a computed
tomography (CT) scan of the head may be
obtained to evaluate evidence of cerebral
edema or hemorrhage

45. Microhematocrit centrifugation
• Using this method with the CBC tube is a more
sensitive method of detection of malaria
infection.
• Does not allow the identification of the
species of Plasmodium.
• To determine species, a peripheral blood
smear must be examined.

46. Fluorescent dyes/ultraviolet indicator
tests
• Several different dyes allow laboratory results
to be obtained more quickly.
• Require the use of a fluorescent microscope.
• Fluorescent /ultraviolet tests may not yield
speciation information.

47. Polymerase chain reaction assay
• Is a very specific and sensitive means of
determining if species of Plasmodium are
present in the blood of an infected individual.
• Not available in most clinical situations.
• Effective at detecting the Plasmodium species
in patients with parasitemias as low as 10
parasites/mL of blood.

48. Lumbar puncture
• If the patient exhibits mental-status changes,
and even if the peripheral smear
demonstrates P falciparum, a lumbar puncture
should be performed to rule out bacterial
meningitis

49. HISTOLOGICAL FINDING

52. PREVENTION

53. ‘ABC’s of Malaria Prevention
• A: Awareness and Assessment of malaria risk
• B: Avoidance of mosquito bites
• C: Compliance with Chemoprophylaxis
• D: Early Detection of Malaria Disease
• E: Effective treatment

55. • Consider Chemoprophylaxis with antimalarials
in patients traveling to endemic areas
• The drug of choice is determined by the
destination of the traveler and any medical
conditions the traveler may have that
contraindicate the use of a specific drug.

56. FIJI GUIDELINES
Duration of prophylaxis:
• Prophylactic drugs should be started at least one
week before travel to endemic area. The drugs
should be continued for the duration of stay and
for a minimum of 4 weeks, preferably 6 weeks,
after leaving the malarious area.
Return from malaria infested area:
• Any illness within a year of return, especially
within three months, might be malaria. Travellers
should be warned to consult a doctor and say
that they have been exposed to malaria if they
fall ill within this period.

57. • Mefloquine 250mg orally once weekly OR
• Chloroquine 300mg (base) orally once weekly and
proguanil 200mg orally once daily OR
• Doxycycline 100mg orally once daily
Caution:
Mefloquine may be associated with neuropsychiatric
side effects.
• It may have antagonistic effects on anticonvulsants and
is not safe in pregnancy. It should be avoided in the
first trimester of pregnancy.
• It is contraindicated in patients with neuropsychiatric
disorder, epilepsy or cardiac conduction defects.
Doxycycline is also to be avoided in pregnancy

58. SOUTH AFRICAN GUIDELINES FOR
THE PREVENTION OF MALARIA
UPDATED 2018

62. Doses for Standby Therapy

63. TREATMENT

64. FIJI GUIDELINES
• If the infective species is not known or if the infection is mixed the
treatment should be as for P.falciparum.
P.FALCIPARUM MALARIA
• As P. falciparum is often resistant to Chloroquine, it should not be
used for treatment.
Adults
Oral therapy
• If no vomiting or impairment of consciousness and patient is able to
swallow:
• Arthemeter and lumafantrine 20 + 120 mg, 4 tablets (child 5-14 kg 1
tablet, 15-24 kg 2 tablets, 25-34 kg 3 tablets) at 0, 8, 24, 36, 48 and
60 hours, making a total of 24 tablets OR
• Quinine Sulphate 600mg orally 8 hourly for 7 days, PLUS EITHER
• Fansidar (pyrimethamine 25mg/ sulphadoxine 500mg) 3 tablets as
single dose on day three OR
• Doxycycline 100mg 12 hourly for 7 days

65. Intravenous Therapy
If patient is seriously ill or cannot tolerate oral medication:
• Artesunate 2.4 mg/kg IV on admission and repeated at 12 hours and 24 hours and
then daily until oral therapy (6 doses as above) can be given OR
• Quinine dihydrochloride as below
• Loading dose: 20mg /kg quinine dihyrochloride (maximum 1.4g of quinine salt)
infused over 4 hours in 500ml of normal saline. Following this it is advisable to give
500ml 5 % dextrose before the next dose of quinine.
• Maintenance dose to start 4 – 8 hours after loading dose is completed: 10mg/kg
(maximum 700mg) in 500ml normal saline (infused over 4 hours) 8 hourly. Give 5%
dextrose in between doses if necessary.
• This is continued until the patient can swallow tablets to complete the 7-day
course.
• A loading dose of 20mg/kg of quinine should not be given if the patient has
received quinine, quinidine or mefloquine during the previous 24 hours. Start on
the maintenance dose of 10mg/kg. Dosage may have to be reduced in the
presence of hepatic and renal dysfunction.
• Quinine can produce hypoglycemia and over hydration may produce pulmonary
oedema.
Quinine is followed by EITHER:
• Fansidar ( Pyrimethamine 25mg/ sulphadoxine 500mg) 3 tablets as a single dose
on day 3 OR
• Doxycycline 100mg 12 hourly for 7 days (Start as soon as possible)

67. BENIGN MALARIA (VIVAX MALARIA)
• Treatment should be aimed at eradicating
blood and liver stages (radical cure).
• Treat as for falciparum malaria and use
primaquine (15 mg orally daily for 21 days
after blood eradication) to eradicate liver
stages

68. GUIDELINES FOR TREATMENT OF
MALARIA IN THE UNITED STATES
APRIL 1, 2019

73. PROGNOSIS
• Most patients with uncomplicated malaria
exhibit marked improvement within 48 hours
after the initiation of treatment and fever free
after 96 hours.
• P. falciparum infection carries a poor prognosis
with a high mortality rate if untreated.
• However, if the infection is diagnosed early
and treated appropriately, the prognosis is
excellent.

74. • Persons living in areas of malaria endemicity may
develop partial immunity to infection with time
and repeated exposure. Limited immunity
reduces the frequency of symptomatic malaria
and also reduces the severity of infection
• Immunity to malaria infection can be lost over
long period of time spent away from endemic
areas with limited exposure.
• As a result, individuals born in malaria endemic
regions who move abroad for work or study and
then return home may be at increased risk for
developing severe malaria and complications of
infection.

75. CONCLUSION
• Malaria is a life threatening disease caused by
Plasmodium Parasites
• Transmitted by female Anopheles mosquito
• It infects the liver and the red blood cells
• P. falciparum being the most threatening
parasite causing vast number of complications
• Symptoms are produced due to the rupture of
red blood cells.

76. REFERENCES
• Ralston, S. H, Penman, I. D, Strachan, M. W. J & Hobson, R. P, 2018,
Davidson's Principles and Practice of Medicine, 23rd edn: Elsevier, Sydney.
• Guidelines for the Treatment of Malaria 3rd Edition, World Health
Organisation, 2015
• Centers for Disease Control and Prevention, Malaria, 2018
• World Health Organisation, Malaria in HIV/Aids patients, 2017
• Suh KN, Kain KC, Keystone JS. Malaria. CMAJ. 2004
• Antibiotic Guidelines, 3rd Edition 2011- Fiji
• World Health Organisation, Malaria in children under five, 2018
• Crutcher JM, Hoffman SL. Malaria. Medical Microbiology. 4th edition.
University of Texas Medical Branch. Chapter 83
• Malaria Site, 2017, Severe Malaria.
• Bartoloni A, Zammarchi L. Clinical aspects of uncomplicated and severe
malaria. Mediterr J Hematol Infect Dis. 2012
• Metanat M. Malaria in Children, Int J Infect. 2015

77. TOXOPLASMOSIS

78. TABLE OF CONTENTS
1. Introduction
2. Epidemiology
3. Transmission
4. Pathophysiology
5. Incubation Period
6. Clinical Presentation
7. Diagnosis
8. Prevention
9. Treatment
10. Prognosis
11. Conclusion
12. References

79. INTRODUCTION
• Toxoplasmosis is caused by infection with the
protozoan Toxoplasma gondi.
• It is an intracellular parasite.
• The infection produces a wide range of clinical
syndromes in humans, land and sea mammals
and various bird species.
• There are 3 major genotypes of T. gondii (type I,
type II and type III). In Europe and the United
States, type II genotype is responsible for most
cases of congenital toxoplasmosis.

80. EPIDEMIOLOGY
• In the United States it is estimated that 11% of the
population 6 years and older have been infected with
Toxoplasma
• Approximately 225,000 cases of Toxoplasmosis are reported
each year, resulting in 5000 hospitalization and 750 deaths,
making T. gondii the 3rd most common cause of lethal
foodborne disease in the United States.
• Toxoplasmosis in patients with AIDS has also been
reported, Imunocompromised patients and also organ
transplantation.
• Toxoplasmosis are more common in southern states, in
African Americans.
• Infection is often highest in areas of the world that have
hot, humid climates and lower altitudes, because the
oocysts survive better in these types of environments

81. TRANSMISSION
Foodborne transmission
Animal-to-human (zoonotic) transmission
Mother-to-child (congenital) transmission
Rare instances of transmission

82. PATHOPHYSIOLOGY

84. • The only known definitive hosts for Toxoplasma gondii are
members of family Felidae (domestic cats and their
relatives). Unsporulated oocysts are shed in the cat’s feces
• Although oocysts are usually only shed for 1-3 weeks, large
numbers may be shed
• Oocysts take 1-5 days to sporulate in the environment and
become infective.
• Intermediate hosts in nature (including birds and rodents)
become infected after ingesting soil, water or plant
material contaminated with oocysts
• Oocysts transform into tachyzoites shortly after ingestion
through cycles of asexual multiplication.
• These tachyzoites localize in neural and muscle tissue and
develop into tissue cyst bradyzoites
• Cats become infected after consuming intermediate hosts
harboring tissue cysts .
• Cats may also become infected directly by ingestion of
sporulated oocysts

85. • Animals bred for human consumption and wild game
may also become infected with tissue cysts after
ingestion of sporulated oocysts in the environment
Humans can become infected by any of several routes:
• Eating undercooked meat of animals harboring tissue
cysts .
• Consuming food or water contaminated with cat feces
or by contaminated environmental samples (such as
fecal-contaminated soil or changing the litter box of a
pet cat) .
• Blood transfusion or organ transplantation .
• Transplacentally from mother to fetus
• 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

86. INCUBATION PERIOD
• T. gondii 10-23 days in adults after ingestion of
uncooked meat
• 5-20 days after ingestion of oocytes from cat
feces.

87. CLINICAL
PRESENTATION

88. Acute Toxoplasmosis in
Immunocompetent Person
• Approximately 80-90% of patients are
asymptomatic. Symptomatic disease may be
characterized as follows:
• Cervical lymphadenopathy – usually
nontender, nodes smaller than 3cm in
diameter.
• Fever, malaise, night sweats and myalgia
• May have a sore throat
• Retinochoroiditis is reported

89. Acute Toxoplasmosis in Hosts who are
Immunodeficient
• CNS Toxoplasmosis – seizure, cranial nerve
deficits, altered mental status, focal neurologic
deficit, headache
• Encephalitis, meningoencephalitis or mass lesion
• Hemiparesis
• Visual changes
• Signs and symptoms similar to those in
immunocompetent hosts
• Flulike symptoms and lymphadenopathy
• Toxoplasmic pneumonitis – symptoms of
pulmonary infection, nonproductive cough,
dyspnea, chest discomfort and fever

90. CONGENITAL TOXOPLASMOSIS
• Most severe when maternal infection occurs
early in pregnancy
• If the mother was infected prior to pregnancy,
there is virtually no risk of fetal infection as long
as she remains immunocompetent
• When the mother is infected with T gondii during
gestation, the parasite may be disseminated
hematogenously to the placenta. Thus, infection
may be transmitted to the fetus transplacentally
or during vaginal delivery

91. • IgM levels may be elevated in newborns with
congenital toxoplasmosis. However, 15-55% of
congenitally infected children do not have
detectable T gondii – specific IgM antibodies at
birth or early infancy
• Retinochoroditis occurs in about 15% of patients
and intracranial calcification develops in about
10%.
• Infected newborns have anemia, rash, fever,
thrombocytopenia, and jaundice at birth
• Microcephaly and hydrocephalus has been
reported.
• Affected survivors may have mental retardation,
seizures, visual defects, spasticity, hearing loss or
other severe neurologic sequelae.

92. OCULAR TOXOPLASMOSIS
• Patients develop retinochoroiditis.
• They have yellowish white, elevated cotton patch
with indistinct margins. The lesion may occurs in
small clusters.
Symptoms include:
• Impaired vision – sudden or gradual, depending
on site of infection
• Blurred vision
• Pain
• Photophobia
• Red eye
• metamorphosia

94. Inactive Retinochoroidal Scar
Secondary to Toxoplasmosis

95. DIAGNOSIS
Direct Detection
• Isolation of T. gondii in blood and body fluids.
• PCR assay test
Indirect Detection – pregnant women and
immunocompromised patients
• IgG detection – within 2 weeks of infection using
ELISA test, IgG avidity and agglutination tests
• Immunoglobulin testing – Fluorescent antibody
test, hemagglutination test, ELISA test and IgG
avidity test

96. Imaging Studies
• CT scan, MRI and Ultrasonography
Diagnostic Procedure for Toxoplasmosis:
• Lumbar puncture
• Brain biopsy
• Lymph node biopsy
• Amniocentesis
Ocular Disease
• Appearance of lesion in the eye, symptoms and
course of disease
• Absence of antibodies rules out the disease
• Ocular fluids and PCR

97. PREVENTION
• Avoid eating raw meat, unpasteurized milk, and
uncooked eggs, oysters, clams, and mussels.
• Wash hands after touching raw meat.
• Wear gloves when gardening or handling soil and wash
hands afterwards.
• Wash fruits and vegetables.
• Avoid contact with cat feces
• Travel to areas of high endemicity (Western Europe,
South America) may increase the risk of exposure
• Avoiding transfusions of blood products from a donor
who is seropositive to a patient who is seronegative
and immunocompromised

98. VACCINE
• The only effective vaccine against toxoplasmosis
is Toxovax, which contains a live attenuated S48
strain and controls congenital infection in sheep.
• Toxovax decreases the abortion rate but does not
eradicate T gondii completely.
• It is expensive and may be changed into a
pathogenic form; for this reason, it is not
appropriate for human use.
• Unfortunately, no licensed vaccine is yet available
for humans

99. TREATMENT

100. FIJI GUIDELINES
• Toxoplasmosis is the most common cause of secondary CNS
infection in patients with AIDS. The standard treatment is
combination therapy with Pyrimethamine and Sulphadiazine.
(a) Primary Therapy
• Sulphadiazine 1 – 1.5g orally / IV 6 hourly PLUS
• Pyrimethamine 50mg orally initially then 25mg orally daily,
• Calcium Folinate can be added to reduce bone marrow suppression,
and the white cell and platelet count must be monitored closely.
• In patients hypersensitive to Sulphonamides substitute
sulphadiazine with Clindamycin* 600mg orally/ IV 6 hourly
• Duration of therapy is for 3 – 6 weeks depending on clinical
response.

101. (b) Prophylaxis
• Relapse is common, so maintenance therapy
is necessary while the patient is
immunosuppressed;
• Co-trimoxazole (Trimethoprim 160mg /
Sulphamethoxazole 800 mg) orally once daily
PLUS
• Pyrimethamine 25mg orally daily OR
• Clindamycin 600mg orally 8 hourly PLUS
• Pyrimethamine AND Folinic Acid

102. MEDSCAPE TREATMENT
GUIDELINES
UPDATED MARCH 8, 2019

103. NONPREGNANT PATIENTS
Immunocompetent, nonpregnant patients typically do not
require treatment. Treatment of nonpregnant patients is
described below.
The 6-week regimen is as follows:
• Pyrimethamine (100mg loading dose orally followed by 25-
50 mg/day) plus sulfadiazine (2-4 g/day divided 4 times
daily) OR
• Pyrimethamine (100-mg loading dose orally followed by 25-
50 mg/day) plus clindamycin (300 mg orally 4 times daily)
• Folinic acid (leucovorin) (10-25 mg/day) should be given to
all patients to prevent hematologic toxicity of
pyrimethamine
• Trimethoprim (10 mg/kg/day) sulfamethoxazole (50
mg/kg/day) for 4 weeks

104. • Sulfadiazine or clindamycin can be substituted
for azithromycin 500 mg daily or atovaquone
750 mg twice daily in immunocompetent
patients or in patients with a history of allergy
to the former drugs

105. PREGNANT PATIENTS
A dosing regimen for pregnant patients is as follows:
• Spiramycin 1 g orally every 8 hours
• If the amniotic fluid test result for T gondii is positive: 3
weeks of pyrimethamine (50 mg/day orally) and
sulfadiazine (3 g/day orally in 2-3 divided doses) alternating
with a 3-week course of spiramycin 1 g 3 times daily for
maternal treatment OR
• Pyrimethamine (25 mg/day orally) and sulfadiazine (4
g/day orally) divided 2 or 4 times daily until delivery (this
agent may be associated with marrow suppression and
pancytopenia) AND
• Leucovorin 10-25 mg/day orally to prevent bone marrow
suppression

106. PATIENTS WITH AIDS
Patients with AIDS are treated with :
• Pyrimethamine 200 mg orally initially,
followed by 50-75 mg/day orally PLUS
• Folinic acid 10 mg/day orally PLUS
• Sulfadiazine 4-8 g/day orally for as long as 6
weeks, followed by lifelong suppressive
therapy or until immune reconstitution.

107. Suppressive therapy for patients with AIDS:
• Pyrimethamine 50mg/day orally plus
• Sulfadiazine 1-1.5 g/day orally plus
• Folinic acid 10 mg/day orally for life or until
immune reconstitution.

108. PATIENTS WITH OCULAR DISEASE
• Prescribed medicine to treat active disease by
their ophthalmologist.
• Depends on the size of the eye lesion, the
location, and the characteristics of the lesion
(acute active vs chronic progressing)

109. PROGNOSIS
• Immunocompetent patients – excellent prognosis.
Lymphadenopathy and other symptoms generally
resolve within weeks of infection
• Immunodeficit patients – often relapses if treatment is
stopped.
• Infants with congenitally acquired toxoplasmosis –
good prognosis and are on average developmentally
identical to noninfected infants by the 4th year of life.
• Toxoplasmic encephalitis and brain abscess – result in
permanent neurologic sequalae, depending on location
of the lesion and extent of local damage and
inflammation.

110. CONCLUSION
• There are no cases of Toxoplasmosis in Fiji.
• Toxoplasmosis is caused by infection with the
protozoan Toxoplasma gondi.
• Cats are the definitive host
• It can cause series of complications
• Can be prevented by hygienic practices and
proper disposal of cat feces.

111. REFERENCES
• Ralston, S. H, Penman, I. D, Strachan, M. W. J & Hobson, R. P, 2018,
Davidson's Principles and Practice of Medicine, 23rd edn: Elsevier,
Sydney.
• Centers for Disease Control and Prevention, Parasites –
Toxoplasmosis (Toxoplasma infection), 2018
• Carlos S. 2006, Toxoplasmosis and HIV, HIV InSitu, University of
California
• Rajesh T G, Toxoplasmosis in HIV-infected patients, UpToDate, 2018
• Antibiotic Guidelines, 3rd Edition 2011- Fiji
• Maria F, 2019, Cerebral Toxoplasmosis, Hospital Medicine, Cancer
Therapy Advisor
• Murat H, 2019, Toxoplasmosis, Practice Essentials, Background,
Pathophysiology.
• McFarland. M. M., Bartlett. M. L. and Davis P. H. 2016. Encephalitis,
Avidscience.

112. THANK YOU !