Internal Medicine for Clinical Medicine Students

1. Clinical Officer General Programme
Jul 2019 Intake
MED 125
PARASITIC INFECTIONS
ML LUBUNDI
Dip, BSc CM,PgCert.ME, mZMLPA, mANCP,mIAPAE,APGD TMSI (IP)
SENIOR LECTURER & DIRECTOR- LUSHES SoH
LUAPULA SCHOOL OF HEALTH SCIENCES
& BUSINESS EDUCATION
SCHOOL OF HEALTH SCIENCES
DEPARTMENT OF CLINICAL MEDICINE

2. Overview of the Lecture
Session
Malaria
Trypanosomiasis
Filariasis
Toxoplasmosis

3. MALARIA

4. Definition
Malaria is a protozoa infection of genus
Plasmodium.
The word ‘malaria’ comes from the Italian
and it means ‘bad air’ that is Mal=bad and
aria= air.
Malaria is a protozoan infection of red
blood cells transmitted by a bite of a blood-
feeding female anopheles mosquito.
(White, 2003).

5. Transmission
 It is transmitted through the bite of an infected
female mosquito belonging to the genus
Anopheles(An)
 In Zambia, there are species that can transmit
human malaria: An. Gambiae, An. Arabiensis,
An. Funestus.
 The differ from many other mosquitoes common
in Zambia by being late-night feeders( thus the
rationale for sleeping under insecticide-treated
mosquito nets[ITNs]).

6. Epidemiology
 Malaria is one of the major public health problems in
Zambia.
 Despite substantial progress made over the past decade,
malaria continues to be a major cause of morbidity and
mortality in the country, resulting in approximately 6
million cases and 2000 deaths (HMIS, 2016).
 Malaria also has an impact on pregnant women.
 In 2018, the high Malaria disease burden resulted in high
morbidity of 680 cases /1000 population, under five child
mortality of 3.9 deaths per 1000 population.

7. Causes
Five species of plasmodium (P.) parasites
cause infections in humans: P. falciparum,
P. vivax, P. malariae, P. ovale, and P.
knowlesi.
Each species has a different biological
pattern through which it affects humans.
The most common species that is clinically
significant and causes the most lethal form
of malaria is P. falciparum.

8. Causes cont’d
In Zambia, P. falciparum accounts for more
than 95% of malaria cases,
 with P. malariae comprising 3%,
P. ovale 2%.
P. vivax is rare in Zambia
No documented cases of P. knowlesi have
been reported in Zambia to date.

9. Pathogenesis
Female anopheles mosquitoes inoculate
sporozoites into humans during a blood
meal.
Sporozoites are carried to the liver,
reproduce asexually, and produce
merozoites that enter the bloodstream,
invade red blood cells (RBCs), and
become trophozoites.

10. Pathogenesis cont’d
After progressively consuming and
degrading intracellular proteins (principally
hemoglobin), trophozoites become
schizonts.
When RBCs rupture, the cycle repeats with
invasion of new RBCs.
In P. vivax or P. ovale infection, dormant
forms called hypnozoites remain in liver
cells and may cause disease 3 weeks to
>1 year later.

11. Pathogenesis cont’d
RBCs infected with P. falciparum may
exhibit cytoadherence (attachment to
venular and capillary endothelium),
rosetting (adherence to uninfected RBCs),
and agglutination (adherence to other
infected RBCs).

12. Pathogenesis cont’d
The result is sequestration of P. falciparum
in vital organs.
Sequestration is central to the
pathogenesis of falciparum malaria but is
not evident in the other three ―benign‖
forms.
With repeated exposure to malaria, a
specific immune response develops and
limits the degree of parasitemia.

13. Pathogenesis cont’d
Over time, pts are rendered immune to
disease but remain susceptible to infection.
Genetic disorders more common in
endemic areas protect against death from
malaria (e.g., sickle cell disease,
ovalocytosis, thalassemia, and G6PD
deficiency).

15. Clinical features
Acute malaria
The feature of the paroxysm are:
 An abrupt onset of an initial‘cold stage‘ associated with a
dramatic rigor(paroxysm) in which the patient visibly
shakes.
 An ensuing =hot stage‘ during which the patient may
have a temperature>40 C, be restless and exitable, and
vomit or convulse.
 Finally, the sweating stage, during which the patient‘s
temperature returns to normal(defervesce) and sleep
may ensue. Such paroxysm can last 6-10 h.

16. Clinical features
Chronic malaria
 The persistence of low-level parasitaemia in the
blood may lead to =chronic malaria‘. Chronic
malaria may resolve, with the onset of partial
immunity, or progress, secondary complications:
 Burkitt‘s lymphoma is childhood tumour common
in areas of high falciparum malaria transmission.
 Hyperreactive malaria splenomegaly
 Quartan malaria nephropathy. P. malariae
infection appears to be a cause of nephritic
syndrome.

17. Clinical features
Uncomplicated malaria
The first symptoms of malaria are
nonspecific;
 the lack of a sense of well-being,
Headache
Fatigue
abdominal discomfort,
muscle aches followed by fever are all
similar to the symptoms of a minor viral
illness.

18. Clinical features
Uncomplicated malaria cont’d
 It should be noted that the patient may not
present with fever but may have a recent history
of fever( during the previous two days).
 This is due to the natural malaria cycle.
 It is equally important to note that fever is a
common symptom for other infections besides
malaria, such as ear infections, measles, and
respiratory infections.
 Malaria nicknamed =Great Imitator‘ because of
this.

19. Clinical features
Severe malaria
 P. falciparum infection in the presence of any life-
threatening condition is considered as severe malaria.
 Some life-threatening conditions include signs and
symptoms such as:
Major:
 Unarousable coma/cerebral malaria: Failure to localize or
respond appropriately to noxious stimuli; coma persisting
for >30 min after generalized convulsion
 Acidemia/acidosis Arterial pH <7.25 or plasma
bicarbonate level of <15 mmol/L; venous lactate level of
>5 mmol/L manifests as labored deep breathing, often
termed ―respiratory distress

20. Clinical features
Major(cont.):
 Severe normochromic, normocytic anaemia:
Hematocrit of <15% or haemoglobin level of <50
g/L (<5 g/dL) with parasitemia of >100,000/L
 Renal failure Urine output (24 h) of _400 mL in
adults or <12 mL/kg in children; no improvement
with rehydration; serum creatinine level of >265
μmol/L (>3.0 mg/dL)
 Pulmonary edema/adult respiratory distress
syndrome: Noncardiogenic pulmonary edema,
often aggravated by overhydration

21. Clinical features
Major(cont.)
 Hypoglycemia Plasma glucose level of <2.2
mmol/L (<40 mg/dL)
 Hypotension/shock Systolic blood pressure of
<50 mmHg in children 1–5 years or <80 mmHg in
adults; core/skin temperature difference of >10C
 Bleeding/disseminated intravascular coagulation:
 Significant bleeding and haemorrhage from the
gums, nose, and gastrointestinal tract and/or
evidence of disseminated intravascular
coagulation

22. Clinical features
Major(cont.)
Convulsions More than two generalized
seizures in 24 h
Haemoglobinuria Macroscopic black,
brown, or red urine; not associated with
effects of oxidant drugs and red blood cell
enzyme defects (such as G6PD deficiency)
Persistent/excessive vomiting
Fluid and electrolytes disturbances

23. Clinical features
Other
 Impaired consciousness: Obtunded but
arousable
 Extreme weakness: Prostration; inability to sit
unaided
 Hyperparasitemia Parasitemia level of >5% in
nonimmune patients (>20% in any patient)
 Jaundice Serum bilirubin level of >50 mmol/L
(>3.0 mg/dL) if combined with other evidence of
vital-organ dysfunction

24. Clinical features
 Blackwater fever: is a massive
haemoglobinuria(the urine becomes very dark) in
the context of malaria.
 The cause is incompletely characterized but in
some case it follows treatment with oxidant dugs
such as primaquine.
 It is more common in patients with G6PD
deficiency or other red cell enzyme
deficiencies(e.g pyruvate kinase).
 In colonial times, blackwater fever was more
common and the mortality much higher.

25. Clinical features
Malaria in pregnancy
Malaria also has an impact on pregnant
women, contributing significantly to
maternal deaths, maternal anaemia,
premature delivery, and low-birth-weight
infant.

26. Diagnosis
Diagnosis based on clinical features alone has
low specificity and often results over-treatement.
 Confirmatory diagnosis plays an important
supportive role in clinical care.
 Parasitological confirmation ( laboratory) is done
by examining either a blood smear/slide or
malaria RDT(rapid diagnosis test).
 Molecular testing can also be used to confirm a
diagnosis of malaria.
o Note: an RDT can be done if microscopy is not
available

27. B/S for Mps
Young trophozoites Old trophozoites

28. Comparisons between RDTs
and Microscopy
Microscopy RDTs
Technically difficult Easy
Requires functional
Equipment
No Equipment Required
Cheap / test Expensive/test
Large working space
required
Minimal space required
Long waiting time Short waiting time
Difficult to use Easy to use
Sequestration not
detected
Able to detect
sequestration
Differentiates parasite Differention in some
High training needs Minimal training needs
Parasite Detection level
 60g/ml
Parasite Detection
Level  100 g/ml
Very sensitive and
specific
Variable sensitivity and
specificity

29. Diagnostic w/out
Supportive investigations:
Investigations to rule out complications:
haemoglobin, blood glucose estimation,
prothrombine time, bilirubin, urea and
creatinine, chest x-ray, FBC.
Investigation for differential diagnosis:
lumbar puncture to exclude meningitis,
blood culture, urine examination, Chest x-
ray.

30. Management
Treatement of uncomplicated malaria
 First line drugs in Zambia is arthemeter-
lumefantrine(AL) given over three days.
 AL is co-formulated at a dosage of 20 mg
arthemether and 120 mg lumefantrine given over
three days.
 The correct dosage for AL is determined by
weight. It is administered at interval of 0, 8, 24,
36, 48, and 60 hours(twice daily for three days).
 Management of fever anti-pyretic drug like
paracetamol or aspirin every 4 to 6 hours until
symptoms resolve.

31. Management
Treatement of uncomplicated malaria(cont.)
 Treatement failure or non-response to treatment(
the anti malaria doesn‘t work even when taken
appropriately).
 In a facility where laboratory facilities are not
available and malaria is still suspected, the
patient should be referred for parasitological
confirmation.
 Administration of oral quinine, on a dose of
10mg/kg body weight every 8 hours for 7 days
using tablets containing 300 mg quinine salt.

32. Management
Severe malaria is a medical emergency, and it
demands urgent clinical assessment and
treatment.
 Initial management of severe malaria
 Clear and maintain airway, where indicated.
 If comatose, position semi-prone or on side.
 Weigh patient(particulary children), if possible, and
calculate dosage per body weight
 Make rapid clinical assessment and look for signs of
meningitis and other conditions.
 Take blood for diagnostic smear/slide or rapid diagnostic
test(RDT), hematocrit, and other laboratory test.

33. Management
Initial management of severe malaria(cont.)
 Exclude hypoglycaemia and monitor blood glucose(every
2 to 4 hours)
 Monitor urine output. If necessary insert urethral catheter.
 Plan first 8 hours of intravenous fluids, including diluents
for antimalarial medicine, glucose therapy, and blood
transfusion, if necessary.
 If auxiliary temperature exceeds 38.5C, take measures to
lower temperature
 In case of convulsions, start anticonvulsant therapy and
monitor patient closely

34. Management of severe Malaria
 Injectable artesunate; Is the drug of choice for
adults and children with severe malaria.
 If injectable artesunate is unavailable,
artemether( IM) or quinine (IV/IM) are
recommended alternatives.
 Following initial parenteral treatment for a
minimum of 24 hours, once the patient can
tolerate oral therapy it is essential to continue
and complete treatment with an effective oral
antimalarial using a full course of an effective
ACT( e.g AL).

35. Management of severe Malaria
Injectable artesunate:
 Dose= 2.4 mg/kg body weight, or 0.24 ml/kg.
 Withdraw into inject intravenously over 5 minutes; if IV
administration is not possible, artesunate may be given
by muscular(IM)
 Note: each vial of injectable must be reconstituted with 1
ml of sodium bicarbonate, which is supplied together with
the vial of artesunate.
 Shake for 2 to 3 minutes until powder is completely
dissolved and the solution is clear.
 Dilute with 2 ml( if IM injection) or 5 ml( if IV injection) of
5% dextrose solution or water for injection or normal
saline(0.9% sodium chloride).

36. Management of severe Malaria
Quinine,
 By IV injection: loading dose: 20 mg/kg body
weight( maximum 1200 mg) diluted in 10 ml/kg of
5% or 10% dextrose
 After 8 hours, give a maintenance dose of 10
mg/kg body weight(maximum 600mg) over 4
hours repeated every 8 hours until patient can
swallow or after coma resolution, then oral
quinine 10 mg/kg body weight every 8 hours to
complete a 7-days course of treatment.

37. Management of severe Malaria
Quinine,
By IM injection: 10 mg/kg body weight
(maximum 1200mg) diluted in saline or
water for injection( to a concentration of
60-100mg salt/ml, repeated after 4 hours
and then every 8 hours.
This should be preferably on anterior thigh.
A maximum of 3 ml should be injected into
one sites.

38. Management malaria in pregnancy
Uncomplicated malaria
 First-line treatment: quinine in the first trimester of pregnancy, AL in
second and third trimesters of pregnancy
 Second-line treatment: quinine should be used in all cases of failure
of first-line treatment.
Severe malaria
 Quinine in the first trimester of pregnancy
 Injectable artesunate in the second and third trimester of pregnancy
Intermittent preventive treatment during pregnancy(IPTp)
 Sulphadoxine-pyrimethamine should be used for IPTp during the
second and third trimesters of pregnancy on a monthly basis at all
scheduled antenatal care visits.

39. Prevention
 Personal Protection Against Malaria Simple measures
to reduce the frequency of mosquito bites in malarious
areas are very important.
 These measures include the avoidance of exposure to
mosquitoes at their peak feeding times (usually dusk and
dawn), but also throughout the night and the use of insect
repellents containing DEET (10 to 35%),suitable clothing,
and insecticide-impregnated bed nets or other materials.
 Chemoprophylaxis Few areas of therapeutics are as
controversial as antimalarial drug prophylaxis.

40. KEY ELIMINATION INTERVENTIONS
 Health Promotion
 Indoor residual spraying (IRS)
 Long Lasting Insecticide-treated mosquito nets
(LLINs)
 Larval source management (LSM)
 Case management, Diagnosis & Treatment
 Integrated community case management (iCCM)
 Malaria in pregnancy (Intermittent Presumptive
Treatment-IPT)
 Mass Drug Administration (MDA)

41. Overview of the Lecture
Session
Malaria
Trypanosomiasis
Filariasis
Toxoplasmosis

42. Overview
The genus Trypanosoma contains many
species of protozoans.
Trypanosoma cruzi, the cause of Chagas‘
disease in the Americas, and the two
trypanosome subspecies that cause
human African trypanosomiasis,
Trypanosoma brucei gambiense and T.
brucei rhodesiense, are the only members
of the genus that cause disease in
humans.

43. African Trypanosomiasis
Sleeping sickness, or human African
trypanosomiasis (HAT), is caused by
flagellated protozoan parasites that belong
to the T. brucei complex and are
transmitted to humans by tsetse flies.
In untreated patients, the trypanosomes
first cause a febrile illness that is followed
months or years later by progressive
neurologic impairmentand death.

44. The parasites and their transmission
The East African (rhodesiense) and the
West African (gambiense) forms of
sleeping sickness are caused, respectively,
by two trypanosome subspecies: T. brucei
rhodesiense and T. brucei gambiense.
These subspecies are morphologically
indistinguishable but cause illnesses that
are epidemiologically and clinically distinct
The parasites are transmitted by blood-
sucking tsetse flies of the genus Glossina.

45. Pathogenesis
 After inoculation, a local inflammatory reaction results in
an itchy, painful chancre(T.b. rhodesiense)
 and regional lymphadenopathy(both T.b. rhodesiense
and T.b. gambiense).
 Invasion of the bloodstream and lymphoreticular system
follows –the haemolymphatic(early) stage.
 Trypanosomes then invade the CNS , producing the
meningoencephalitic(late) stage of the disease.
 Trypanosomes escape the most immunological response
by changing their surface antigens(antigenic variation).

46. Epidemiology
 The trypanosomes that cause sleeping sickness
are found only in Africa.
 Approximately 50 million persons are at risk of
acquiring HAT, and tens of thousands of new
cases occur every year.
 Humans are the only reservoir of T. b.
gambiense, which occurs in widely distributed
foci in tropical rain forests of Central and West
Africa.
 Trypanotolerant antelope species in savanna and
woodland areas of Central and East Africa are
the principal reservoir of T. b. rhodesiense.

47. Clinical features
 A painful trypanosomal chancre appears in some patients
at the site of inoculation of the parasite.
 Haematogenous and lymphatic dissemination (stage I
disease) is marked by the onset of fever.
 Typically, bouts of high temperatures lasting several days
are separated by afebrile periods.
 Lymphadenopathy is prominent in T. b. gambiense
trypanosomiasis.
 Cervical nodes are often visible, and enlargement of the
nodes of the posterior cervical triangle, or Winterbottom’s
sign, is a classic finding.
 Pruritus and maculopapular rashes are common.

48. Clinical features
 A CNS invasion (stage II disease)
 A picture of progressive indifference and daytime
somnolence develops (hence the designation―sleeping
sickness‖), sometimes alternating with restlessness and
insomnia at night.
 A listless gaze accompanies a loss of spontaneity, and
speech may become halting and indistinct.
 Extrapyramidal signs signs may include choreiform
movements, tremors, and fasciculations.
 In the final phase, progressive neurologic impairment
ends in coma and death.

49. Clinical features
 Persistent tachycardia unrelated to fever is
common early in the course of T. b. rhodesiense
trypanosomiasis
 Death may result from arrhythmias and
congestive heart failure before CNS disease
develops.
 In general, untreated T. b. rhodesiense
trypanosomiasis leads to death in a matter of
weeks to months, often without a clear
distinction between the hemolymphatic and CNS
stages.

50. Diagnosis
 Examination of fluid from the chancre, thin or
thick blood smears, lymph node aspirates, bone
marrow biopsy specimens, or cerebrospinal fluid
(CSF) samples can reveal the parasite.
 CSF should be examined whenever the
diagnosis is being considered.
 Increased opening pressure, increased protein
level, and increased mononuclear cell counts
are common.
 Parasites can be visualized in the sediment of
centrifuged CSF.

51. Treatment
 Treatment is toxic and must be closely supervised.
Stage I disease
East African:
 Suramin (a test dose of 100–200 mg followed by 20 mg/kg IV on
days 1, 5, 12, 18, and 26).
 Fever, photophobia, pruritus, arthralgias, skin eruptions, and renal
damage can occur.
 Severe reactions (shock, seizures) can be fatal.
West African:
 Pentamidine (4 mg/kg daily IM or IV for 10 days).
 Serious adverse reactions include nephrotoxicity, abnormal liver
function, neutropenia, hypoglycaemia, and sterile abscesses.
 Suramin is the alternative treatment.

52. Treatment
Stage II disease
East African:
 Melarsoprol (2–3.6 mg/kg daily in 3 divided doses for 3
days; 1 week later, 3.6 mg/kg per day in 3 divided doses
for 3 days; 1 week later, the latter course repeated).
 To reduce melarsoprol-induced encephalopathy,
administer prednisolone (1 mg/kg up to 40 mg daily,
starting 1–2 days before the first dose of melarsoprol and
continuing through the last dose).
West African:
 Eflornithine (400 mg/kg per day in 4 divided doses for 2
weeks) is the first-line agent, with melarsoprol as an
alternative.

53. Prevention
Eradication of vectors and drug treatment
of infected humans
Individuals can reduce their risk of
acquiring trypanosomiasis by avoiding
areas known to harbour infected insects,
by wearing protective clothing, and by
using insect repellent.
Chemoprophylaxis is not recommended,
and no vaccine is available to prevent
transmission of the parasites.

54. Overview of the Lecture
Session
Malaria
Trypanosomiasis
Filariasis
Toxoplasmosis

55. Filariasis due to wucheleria bancrofti

56. Definition
Filariasis is a disease group affecting
humans and animals, caused by filariae;
Infection with the filarial worms Wuchereria
bancrofti is associated with clinical
outcomes ranging from subclinical infection
to hydrocele and elephantiasis.

57. Transmission
W. Bancrofti is transmitted by night-bitting
culicine or anopheline mosquitoes in most
areas.
The adult worms, 4-10 cm in length, live in
the lymphatics, and the females produce
microfilariae which circulate in large
members in the peripheral blood, usually
at night.

58. Epidemiology
The infection is widespread:
In tropical Africa,
On the North African coast,
In coastal areas of Asia,
Indonesia and northern Australia,
The South Pacific islands,
The West Indies
 In North and South America.

59. Pathogenesis
 The principal pathologic changes result from
inflammatory damage to the lymphatics, which is
caused by adult worms and not by microfilariae.
 Adult worms live in afferent lymphatics or sinuses
of lymph nodes and cause lymphatic dilatation
and thickening of the vessel walls.
 Lymphedema and chronic-stasis changes with
hard or brawny oedema develop in the overlying
skin.
 Lymphatic obstruction results, and, despite
collateralization of the lymphatics, lymphatic
function is compromised.

60. Clinical features
 The most common presentations of the lymphatic
filariases are asymptomatic (or subclinical)
microfilaremia, hydrocele , acute adenolymphangitis
(ADL), and chronic lymphatic disease.
 ADL is characterized by high fever, lymphatic
inflammation (lymphangitis and lymphadenitis), and
transient local edema.
 Regional lymph nodes are often enlarged, and the entire
lymphatic channel can become indurated and inflamed.
 Concomitant local thrombophlebitis can occur as well.

61. Clinical features
 The genital lymphatics occurs, this genital
involvement can be manifested by funiculitis,
epididymitis, and scrotal pain and tenderness.
 In endemic areas, another type of acute
disease—dermatolymphangioadenitis
(DLA)—is recognized as a syndrome that
includes high fever, chills, myalgias, and
headache.
 Edematous inflammatory plaques clearly
demarcated from normal skin are seen.
 Vesicles, ulcers, and hyperpigmentation may
also be noted.

62. Clinical features
 Entry lesions, especially in the interdigital area, are
common.
 DLA is often diagnosed as cellulitis. If lymphatic damage
progresses, transient lymphedema can develop into
lymphatic obstruction and the permanent changes
associated with elephantiasis.
 Brawny oedema follows early pitting oedema, and
thickening of the subcutaneous tissues and
hyperkeratosis occur.
 Fissuring of the skin develops, as do hyperplastic
changes.
 Hydroceles may develop; in advanced stages, this
condition may evolve into scrotal lymphedema and
scrotal elephantiasis.

64. What can you?

66. Diagnosis
 Detection of the parasite is difficult, but
microfilariae can be found in peripheral blood,
hydrocele fluid, and occasionally other body
fluids.
 Timing of blood collection is critical.
 Two assays are available to detect W. Bancrofti
circulating antigens, and PCR has been
developed to detect DNA .
 High-frequency ultrasound of the scrotum or the
female breast can identify motile adult worms.
 Pts have eosinophilia and elevated IgE levels.

67. Treatment
 Diethylcarbamazine (DEC) given at 6 mg/kg daily
for 12 days is the standard regimen, but one
dose may be equally efficacious.
 An alternative is Albendazole (400 mg bid for 21
days), but this drug may be less effective than
DEC.
 An 8-week course of daily Doxycycline, which
targets Wolbachia endosymbionts, has
significant macrofilaricidal activity and sustained
microfilaricidal activity, as does a 7-day course of
daily DEC/Albendazole.

68. Treatment
Side effects of DEC treatment include
 Fever
 Chills,
 Arthralgias,
 Headaches,
 Nausea, and vomiting.
These usually occur within 24-36 hours of the
first dose of DEC.
Antihistamines or corticosteroids may be
required to control these allergic phenomena.

69. Prevention
Mosquito control or personal protective
equipment can minimize bites.
Mass annual distribution of albendazole
with DEC or ivermectin for community-
based control reduces microfilaremia and
interrupts transmission.

70. Overview of the Lecture
Session
Malaria
Trypanosomiasis
Filariasis
Toxoplasmosis

71. Overview
 Toxoplasma gondii is an intracellular
protozoan parasite found widely in the
environment
 Reservoirs include cats, birds and
domesticated animals
 Transmission occurs when humans ingest
oocysts from contaminated soil or tissue cysts
from undercooked meat.
 Acute infection with T. gondii during pregnancy
results in transmission to the fetus in about one-
third

72. Pathogenesis
Both humoral and cellular immunity are
important, but infection commonly
persists.
Such lifelong infection usually remains
subclinical.
Compromised hosts do not control
infection; progressive focal destruction
and organ failure occur.

73. Clinical features
Disease in immunocompetent hosts is
usually asymptomatic and self-limited and
does not require therapy;
 Cervical lymphadenopathy is the most
common finding; nodes are non tender
and discrete.
Generalized lymphadenopathy can occur.
Fever, headache, malaise, and fatigue are
documented in 20–40% of pts with
lymphadenopathy.

74. Clinical features
Immunocompromised pts, including those
with AIDS (with CD4 < 100)and those
receiving immunosuppressive treatment
for lymphoproliferative disorders, are at
greatest risk.
 Most clinical disease is due to reactivated
latent infection.

75. Clinical features
In Immunocompromised Patients
1. CNS: principal site of involvement.
Findings include encephalopathy,
meningoencephalitis, and mass lesions.
 Pts may exhibit changes in mental status,
fever, seizures, headaches, aphasia and
focal neurological deficits common.

76. Clinical features
In Immunocompromised Patients
2. Pneumonia: Dyspnoea, fever, and non
productive cough can progress to
respiratory failure.
Toxoplasma pneumonia is often confused
with Pneumocystis pneumonia.
3. Miscellaneous sites: GI tract, pancreas,
eyes, heart, liver

77. Clinical features
Congenital infection, severe disease,
manifesting as hydrocephalus,
microcephaly, mental retardation, and
chorioretinitis, is more common the earlier
the infection is contracted.

78. Clinical features
Ocular infection:
Chorioretinitis, blurred vision, scotoma,
photophobia, and eye pain are
manifestations of infection.
On examination, yellow-white cotton-like
patches with indistinct margins of
hyperemia are seen.
Older lesions appear as white plaques
with distinct borders and black spots.

79. Diagnosis
 Acute toxoplasmosis can be diagnosed by the
demonstration of tachyzoites in tissue or by
documentation of the simultaneous presence of
serum IgM and IgG antibodies to T. gondii.
 In AIDS pts, the infection is diagnosed
presumptively on the basis of clinical
presentation and a positive test for IgG antibody
to T. gondii.
 In these pts, CT or MRI of the brain shows
lesions that are often multiple and contrast
enhancing.

80. Diagnosis
 Congenital toxoplasmosis is diagnosed by PCR
of the amniotic fluid (to detect the B1 gene of
the parasite) and by the persistence of IgG
antibody or a positive IgM titer after the first
week of life; IgG antibody determinations should
be repeated every 2 months.
 Ocular toxoplasmosis is diagnosed by the
detection of typical lesions on ophthalmologic
examination and the demonstration of a positive
IgG titer.

81. Management
Congenital infection: daily pyrimethamine
(0.5–1 mg/kg) and sulfadiazine (100
mg/kg) for 1 year.
If infection is diagnosed and treated early,
up to 70% of children can have normal
findings at follow-up evaluations.
Ocular disease: pyrimethamine and
sulfadiazine or clindamycin for 1 month

82. Management
Immunocompromised pts:
Co-trimoxazole (Septrin) 3-4 tabs bd (1 tab
= 480 mg)
If < 50 kg, use 3 tabs bd
If > 50 kg, use 4 tabs bd
 For very sick patients, use steroids
Prednisolone 30 mg bd

83. Chemoprophylaxis
 The risk of disease is very high among AIDS pts who are
seropositive for T. gondii and have a CD4+ T lymphocyte
count of <100/μL.
 Trimethoprim-sulfamethoxazole: 960 mg OD should be
given to these pts as prophylaxis against both
Pneumocystis pneumonia and toxoplasmosis.
 Primary or secondary prophylaxis can be stopped if, after
institution of antiretroviral treatment, the CD4+ T
lymphocyte count increases to >350/μL and remains
above that cutoff for 6 months.

84. Personal Protection Measures
Toxoplasma infection can be prevented by
avoiding undercooked meats and oocyst-
contaminated materials (e.g., cats‘ litter
boxes).

85. END
Roots of education are bitter, but
the fruit is sweet