Blood and Tissue Protozoa

Blood and tissue protozoa of man
Organism Disease Epidemiology

T. brucei sleeping sickness Central Africa: 10x106
T. cruzi Chagas’ disease South/Central America:
20x106
L. donovani visceral leishmaniasis Asia: 10x106
L. tropica cutaneous leishmaniasis Mediterranean: 5x106
L. Braziliensis mucocutaneous South/Central America:
and other leishmaniasis 10x106
Blood and tissue protozoa of man

P. falciparum, malaria Tropics and subtropics:
P. ovale, P. vivax, 200x106
P. Malariae
T. gondii Toxoplamosis world wide:

opportunistic
B. microti babesiosis, anemia North America

and Europe
Trypanosomiasis
African trypanosomiasis (sleeping sickness)

T. brucei, rhodesiense
T. brucei gambiense
American trypanosomiasis (Chagas’ disease)

T. cruzi
Trypanosome
general morphology
African trypanosomiasis
geographic distribution of T. brucei
Trypanosoma brucei
morphological forms
Epimastigote (crithidial
form) in the insect
Trypomastigote
(trypanosomal form) in
the mammalian host
Trypanosoma brucei
life cycle
Symptoms of African
trypanosomiasis
stage organ Involved symptoms

bite reaction skin non pustular, itchy, painful
chancre; no scar
blood circulation malaise, lassitude,
parasitemia
and lymph nodes insomnia, fever, edema,
lymphadenopathy
personality changes,
CNS stage CNS, heart shuffling gait, lack of
interest, tremulous speech,
mental retardation,
sleepiness, cardiac failure.
T. Brucei :
Winterbottom’s sign
T. Brucei :
coma
T. Brucei :
pathology and Immunology
Immunology
Pathology  Antibodies are not
 Inflammation protective due to
 Type III hypersensitivity antigenic change
 Antigenic change
 Polyclonal B cell
expansion; Hyper-IgM
 CNS damage by the
organisms
 hypocomplementemia
 Immunosuppression
 RE stimulation
T. Brucei :
antigenic variation
T. Brucei :
diagnosis
 History of travel and

fly-bite
 Symptoms
 Blood smear and/or
CSF
 Anionic support
concentration
 Bioassay (mouse)
 EIA, IF
T. Brucei :
Prevention and treatment
Prevention Treatment
 No effective vaccine
 Acute disease
(changing VSG)
 Suramin
 Tsetse fly control
 Pentamidine
 Insect-bite
 Chronic (CNS)
avoidance
disease
 Suramin or  Melarsoperol (arsenic)
pentamidine
American trypanosomiasis
geographic distribution
American trypanosomiasis
Etiologic agent (T. cruzi)
T. cruzi :
life cycle
Reservoir
Armadillo, opossum,
raccoon, dog cat, and
other animals
T. cruzi :
Transmission
Triatoma
sordida,
T. infestans,
Panstrongylus
magistus,
Rhodnius
prolixus,
etc.
kissing bugs
cone nose bugs
T. cruzi :
Transmission
Chagas' disease:
pathology
 Direct Inflammatory response

 Chaga-toxin
 damage to infected cells
 Destruction of autonomic nerve
ganglions
 Products of humoral and CMI
Chagas' disease:
Immunology
 Antibody kills, but not eradicate T. cruzi

 CMI of some protective value
 Activation macrophages kill the organism
 RE stimulation
 Immunosuppression
Chagas' disease:
diagnosis
 History of travel and
sometimes cardiac
problems
 Romamna’s sign or
chagoma
 Organisms in the
chagoma exudate,
lymph node aspirate or
blood
 Bioassay in mice or
uninfected triatoma
Chagas' disease:
prevention and treatment
 Nifurtimox effective in acute stage

 Benznidizol may be of value in
chronic stage
 Avoid and control the insect
population
 No vaccine
Leishmaniasis
Leishmaniasis

L. donovani visceral leishmaniasis Asia: 10x106
L. tropica cutaneous leishmaniasis Mediterranean: 5x106
L. Braziliensis mucocutaneous South/Central America:
and other leishmaniasis 10x106
Leishmania
morphology
 Amastigote (leishmania)
seen in the mammalian
host
 Promastigote
(leptomonad) seen in
sand fly
Leishmania
life cycle
vector
Human
cycle
Animal
reservoir
Leishmania
symptoms
type organ Involved symptoms
liver, spleen, No bite reaction; lymphadenopathy,

visceral bone marrow, splenomegaly and hapatomegaly;
lymph nodes, parasitemia, chills and fever;
skin darkening of skin
cutaneous
centrifugally growing papular lesion
skin
with central crusting; heals
spontaneously, permanent scar
muco- initially same as cutaneous lesion
Skin and mucoid
cutaneous tissue but it does not heal: necrosis of
mucoid tissue; metastasis to distant
mucoid tissues; very disfiguring
Visceral Leishmania
 1-4 months: fever chills,

diarrhea, dysentery
 Progressive hepato-
splenomegaly
 skin hyperpigmentation
 Death, if untreated
Cutaneous leishmaniasis
Disseminated cutaneous
leishmaniasis
Mcutaneous
leishmaniasis
Leishmaniasis
diagnosis
 History
 Lesions or
symptoms
 Organisms in the
lesion
 Montenegro test
(type IV hypersensitivity)
Leishmaniasis
Pathogenesis and immunology
 Damage due to CMI

 Leishmanial proteoglycan
 Leukopenia with monocytosis and
lymphocytosis
 immunosuppression
 Interferon and TNF are protective
Leishmaniasis
Preventions and treatment
 No vaccine
 Control of sand fly and infected animals
 avoidance of sand fly
 Pentosam (antimony gluconate)
Malaria
 Plasmodium falciparum
 Plasmodium vivax
 Plasmodium ovale
 Plasmodium malariae
Malaria
Malarial parasites
morphology
 Malignant
tertian
 Benign tertian
 Ovale tertian
 Quartan
Malarial parasites
life cycle
Malarial symptoms
type organ Involved symptoms

tertian spleen, headache, lassitude, vague aching of bones
(vivax and liver, and joints, chills and high fever (103-106 F),
ovale) erythrocytes nausea and vomiting, convulsion, euphoria,
profuse sweating. Symptoms every other day
systemic and last 8-12 hours . Spontaneous recovery
falciparum same as above but no tertian pattern: there

(malignant may be daily spiking; no spontaneous recovery
tertian) and ultimately fatal. Renal & CNS involvement
quartan same as tertian, but paroxysm occurs every

(malariae) three days (2 clear days)
Malarial paroxysm
Malarial diagnosis
 Travel history
 symptoms
v
f
 Blood smear
o m
Malaria
control and treatment
 Control
 Control mosquito population
 Mosquito netting
 Treatment:
 Quinine derivatives
 P. falciparum often drug resistant
 Quinine can be use prophylactically
Babesiosis
geography and etiology
 Etiologic agent is Babesia microti

 Zoonotic infection
 Deer are primary reservoir
 Cases reported in north-eastern part
of the US and Europe
Babesiosis
morphology
 Similar to malarial
parasite, but no
schizonts or
gametocytes
 Up to four
trophozoites per
cell
Babesia microti
life cycle
Babesiosis
symptoms
 Mild chills and fever

 Hemolytic anemia
 Jaundice
 Hepatomegaly
No malarial paroxysm
Babesiosis
diagnosis
 Symptoms
 History of tick bite
No malarial paroxysm
 Characteristic
organisms in blood
Babesiosis
prevention and treatment
 Avoid tick bites
 Recovery may be
spontaneous
 Clindamycin with
quinine is effective
Toxoplasmosis
 The etiologic agent T.gondii is

distributed worldwide
 Most of the populations is
seropositive
 Threat to immunosuppressed and

unborn
Toxoplasma gondii
morphology
 Intracellular
(macrophage)
parasite
 3-6 x 1-2 m
Toxoplasma gondii
life cycle
Toxoplasmosis
symptoms
host status symptoms
prenatal 1-5% aborted, 8-10% serious brain

and eye damage, 10-13% less serious
visual and mental problems, ~70%
late visual and mental problems
normal adult flue-like
immuno- parasitemia, cysts in visceral

compromised organs, eye, and CNS, often fatal
Toxoplasma gondii
retinitis
Toxoplasma gondii
hydrocephalus
Toxoplasma gondii
encephalitis
Toxoplasma gondii
Pathology and Immunology
Pathology Immunology

 Both humoral and
Growing mass
CMI are stimulated
 CMI  CMI is protective
Toxoplasma gondii
Diagnosis and treatment
Diagnosis Treatment
 History  Sulphonamide or
 CT scan pyremethamine
 Tonsil or lymph node  Spyramycin
biopsy
Pneumocystis carinii
Not a protozoa, Treatment

it’s a yeast
 trimethoprim
 Opportunistic  sulphamethoxazole
 Major cause of
pneumonia among
AIDS patients
Facultative protozoan
parasites
Negleria Fowleri Acanthamoeba
 Rare  Rare
 In warm spas  In soil
 Causes encephalitis  pharengitis,
occasionally
encephalitis

Blood and Tissue Protozoa

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Blood and Tissue Protozoa

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Blood and tissue protozoa of man

Organism Disease Epidemiology

Organism Disease Epidemiology

T. gondii Toxoplamosis world wide:

B. microti babesiosis, anemia North America

African trypanosomiasis (sleeping sickness)

American trypanosomiasis (Chagas’ disease)

stage organ Involved symptoms

 History of travel and

 Direct Inflammatory response

 Antibody kills, but not eradicate T. cruzi

 Nifurtimox effective in acute stage

Organism Disease Epidemiology

type organ Involved symptoms

liver, spleen, No bite reaction; lymphadenopathy,

 1-4 months: fever chills,

 Damage due to CMI

type organ Involved symptoms

falciparum same as above but no tertian pattern: there

quartan same as tertian, but paroxysm occurs every

 Etiologic agent is Babesia microti

 Mild chills and fever

 Avoid tick bites

 The etiologic agent T.gondii is

 Threat to immunosuppressed and

host status symptoms

prenatal 1-5% aborted, 8-10% serious brain

normal adult flue-like

immuno- parasitemia, cysts in visceral

Not a protozoa, Treatment

Negleria Fowleri Acanthamoeba

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