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Protozoa
Dr Mohiedd n M Abdul Fattah
Luminal protozoa
. Intestinal amoebae Entamoeba histolytica and E.dispar. . Intestinal flagellates Giardia
intestinalis. . Urogenital flagellates Trichomonas vaginalis . Intestinal apicomplexans coccidia
Cryptosporidium parvum and C hominis . Intestinal ciliates Balantidium coli
Patterns of protozoan life cycle
Blood and Tissue protozoa
.Blood flagellates Trypanosoma and Leishmania. .Blood apicomplexans coccida Plasmodium
malaria parasites and Toxoplasma
gametocytes
GAMETOGONY
zygote
SPOROGONY
merozoites
MEROGONY
sporozoites
Amoebae E. histolytica and dispar
A. Biology
Final host Human. Habitat Colon Exit stage trophozoites, precysts, binucleate and
Quadrinucleate cysts in feces. Basic morphology trophozoite m amoeboid, and round cyst m.
Amoebae Basic Morpology and Life Cycle
Entamoeba histolytica large intestine but can invade extraintestinal sites
Amoebae Life cycle
. Trophozoites colonize large intestine feed on bacteria and debris replicate by binary fission
. Trophozoite rounds up to form cyst secretion of cyst wall aggregation of ribosomes
chromatoid bodies rounds of nuclear division occur p nuclei survive weeks to months
Amebae E. histolytica and dispar
B. Epidemiology Distribution both are worldwide
of E. histolytica cases are symptomatic, severe infections occurs in pregnant women, young
children, the malnourished and people on steroids.
Transmission
. Intermediate host none . Reservoir host none . Infective stage nuclei cyst. It remains viable
in damp cool conditions up to months . Mode of infection ingestion of food and drinks
contaminated by the infective stage
C.Host
r sit r l tionshi
The nonpathogenic E. dispar is non invasive. Only E histolytica is invasive and symptomatic,
but under certain condition it is non invasive and non symptomatic. Noninvasive condition .
Amebae colonize on mucosal surface without inducing symptoms Asymptomatic cyst passer
or it induces . Nondysenteric diarrhea .
Invasive amebiasis
Invasive ondition a Amebae invade mucosa ulcer Dysentery. b Via blood invasion or by
direct extension Metastasis extraintestinal amebiasis. . Primarily liver amebic abscess . Other
sites skin, lung and brain. Amebafree stools are common in such situations.
Colitis is the ost ommon form of disease associated with amoebae
Amoeba invade mucosa and erode through laminia propria causing characterisitic flask
shaped ulcers contained by muscularis
Invasive intestinal phase continued
ulcer enlar ement p severe dysentery perforation of intestinal wall p peritonitis local
abscesses o bacterial infections occasional ameboma amebic ranuloma cessation of cyst
production
ameboma inflammatory thickening of intestinal wall around the abscess can be confused
with tumor
Ulceration can lead to secondary infection and extraintestinal lesions
Extraintestinal Amebiasis
metastasis via blood stream primarily liver portal vein other sites less frequent amebafree
stools common hi h antibody titers
Amebic Liver Abscess
chocolatecolored pus necrotic material usually bacteria free lesions expand and coalesce
further metastasis, direct extension or fistula
Cutaneous Amebiasis
intestinal or hepatic fistula mucosa bathed in fluids containing trophozoites perianal ulcers
urogenital eg, labia, vagina, penis
D. Diagnosis
D.Intestinal stool examination To detect cysts and/or trophozoites by microscopy Or to detect
antigen in stool specific E. histolytica lectin by ELISA. This differentiates histolytica from
dispar Lower endoscopy to see lesions, take aspirate, or biopsy ii.Extraintestinal hepatic
Serology to detect amobic lectin antigen or its antibodies Imaging CT, MRI, Sonar Abscess
aspiration non suppurative reddish brown liquid full of trophozoites. Only applied on clinical
cases to differentiate between amoebic and bacterial abscesses
. Trophozoite
imaging CT, MRI, Sonar They do not differentiate between bacterial and amoebic abscess
. Precyst . Binucleate cyst. . Quadrinucleate cyst
E.Treatment
. Asymptomatic cyst pasers dilxanide furoate mg tds for days, iodoquinol or paromomycin mg
tds for days endemic areas Mass treatment. . symptomatic metronidazole mg tds for days or
tinidazole followed by lumenal agents dilxanide furoate mg tds for days . drain liver abscess
only with high probability of rupture
Amoebae E. histolytica
F.Control Personal hygiene, Food sanitation proper disposal of human sewage.
Pathogenic Free Living Amoebae
Mohiedden M AbdulFattah
Classification
Schizopyrenida Amoeboflagellates
Naegleria fowleri
Acanthpodina
Acanthamoeba culbertsoni.
Ecology of Naegleria fowleri
It grows fastest at oC, in water piped above ground, swimming and medicinal pools,
acquarium, and in sewage. stages in the life cycle . Trophozoite is an amoeboid feeding
stage
Biology in the human host
Naegleria is pathogenic to human host when gets access to him. Habitat in man brain
tissues and meninges. Exit stage None, but trophozoites can be recovered from brain tissue
biopsy and CSF. Flagellated form from CSF only. Three stages exist in its life cycle
amoeboid trophozoite, flagellate and cyst. Cysts exist only in the environment
. All stages are characterized by a single nucleus with a large karyosome and no visualised
peripheral chromatin. . The ameboid transforms into a pearshaped flagellate with two flagella
at the end if placed in distilled water or CSF
. In desiccation or low nutrients, amoeboid encysts. . The cyst reverts back to trophozoite in
favorable cases. . Cysts exist only outside human.
Epidemiology
Distribution freshwater habitats and rarely moist soil throughout the world. Human infections
are quite rare and are acquired directly from the environment. Transmission No
humantohuman transmission or vector transmission. . Intermediate host no . Reservoir host
no . Infective stage Trophozoites. . Mode of infection During swimming in warm or heated
waters, the trophozoites enter through the olfactory neuroepithelium in the nasal cavity
migrate along the olfactory nerves into the brain.
Hostparasite relationship
Naegleria produces a fulminate, almost always fatal, acute meningoencephalitis primary
amoebic meningoencephalitis PAM in healthy children and young adults. There is a rapid
progression from headache and fever to coma, seizures and death.
Diagnosis
Unless diagnosed, treated early, infection is fatal. Cloudy CSF shows neutrophils, glucose,
and proteins. Wet microscopy of CSF motile amoebae without bacteria. Biopsy from brain
tissues stained by Wright or by monoclonal PAP stains may help, but it is almost
always too late.
Treatment
only documented survivors
Amphotericin B .mg/kg IV daily for d and mg/kg/d for d or intrathecally by lumbar catheter .
mg for d then mg every other day for d.
Health education to avoid bathing in .stagnant fresh water lake, .pools contaminated with
sewage, .underchlorinated swimming pools. Chloramination, ammonia and chlorine to the
water, is more effective in practice.
control
Acanthamoeba
Acanthamoeba is group of amoebae unrelated to Naegleria, but also freeliving. It is
infectious, causing two diseases .Granulomatous amoebic encephalitis GAE It occurs in
immunesuppressed patients, usually secondary to infection elsewhere in the body e.g. skin
ulceration. .Amoebic Keratitis AK is a severe corneal infection, among the immune
competent hosts
Biology
It is free living, but can infects man Habitat in human nostrils and throats skin, lung tissues,
and brain. Exit diagnostic stage No... But trophozoites and cyst can be found in histological
sections No flagellated form.
Morphology and life cycle
Trophozoite um with spine like pseudopodia. Cyst double walled, polygonal or spherical um
Epidemiology
Distribution Throughout the world. .In soil fresh, brackish, and sea water sewage swimming
pools .Contact lens equipment and in medicinal pools .Dental treatment units .Dialysis
machines .Heating, ventilating, and air conditioning systems
Transmission
Transmission No humantohuman or vector transmission.
Intermediate host no. Reservoir host no. Infective stage Trophozoites and cysts. Mode of
infection The trophozoites and cysts can enter human through .eye, .nasal passages to the
lower respiratory tract, or .through ulcerated skin .to CNS via blood.
Host parasite relationship, continued
Disseminated infections of various other tissues including lung pneumonitis and skin
ulceration. In healthy individuals, The prominent disease is Acanthamoeba keratitis AK, A
potentially sightthreatening eye infection, especially in patient with contact lens. In immune
copromised Chronic granulomatous encephalitis GAE
Autopsy of GAE
The autopsy revealed extensive necrotizing granulomatous encephalitis with subependymal
necroinflammatory process.
Tissue section c of the brain were made and stained with HampE.
Lesions in acanthamoebic infection
Acanthamoebic skin ulceration
Acanthamoebic keratitis
Acanthamoebic granuloma in brain tissues
Diagnosis
. It is difficult . Amebas not yet detected in spinal fluid . Cysts and trophozoites are detected
in brain biopsy GAE or in corneal scrapings keratitis.
Treatment . Some success in treating amebic keratitis has been obtained with propamidine
isethionate Brolene. . Surgery is often needed to correct the loss of vision.
Control
. Health education . Care of skin lesions, . use of sterilized saline for contact lens.
Luminal flagellates Basic morphology and life cycle
Urogenital flagellate Trichomonas vaginalis Intestinal flagellates small inrtestine Giardia
lamblia
Giardia lamblia
A. Biology
Final host man Habitat small intestine. Exit diagnostic stage Trophozoite and cyst. Basic
morphology and life cycle
B. Epidemiology of Giardiasis
Distribution Worldwide, more prevalent in warm climates, and in children. Transmission.
Intermediate host no. Reservoir host no. Infective stage cyst. Mode of infection By the
ingestion of cysts in contaminated water, food, or by the fecaloral route hands or fomites,
autoinfection .
C. Giardiasis Hostparasite relationship
Giardia never invade intestinal mucosa Asymptomatic infection to severe diarrhea and
malabsorption. Acute infection develops after days and usually lasts to weeks Diarrhea,
abdominal pain, bloating, nausea, and vomiting occur. Chronic infection Symptoms recur
with malabsorption and debilitation.
D. Diagnosis of Giardiasis
Identification of cysts or trophozoites in the feces or in duodenal aspirate Enterotest.
Detection of antigens in stool by ELISA, or parasites by immunofluorescence.
E. Treatment of Giardiasis
Metronidazole flagyl ,tinidazole Fasygin or Nitazoxanide cryptonaz. F. Control Environmental
sanitation and personal hygiene
Trichomonas vaginalis
A. Biology Final host man Habitat In the female, lower genital tract and the male urethra and
prostate. Exit diagnostic stage Trophozoite no cyst stage. Basic morphology and Life cycle
B. Epidemiology of Trichomoniasis
Distribution Worldwide. Higher prevalence among persons with multiple sexual partners.
Transmission Intermediate host no. Reservoir host no. Infective stage trophozoite. Mode of
infection By direct contact during sexual intercourse.
C. Hostparasite relationship . In female Vaginitis with a purulent discharge is the prominent
symptom. It can be accompanied by vulvar and cervical lesions, abdominal pain, dysuria and
dyspareunia. . In men, the infection is frequently asymptomatic occasionally, urethritis,
epididymitis, and prostatitis can occur.
D. Diagnosis
Detecting actively motile organisms in wet smears from vaginal, urethral or prostatic
secretions. Direct immunofluorescent antibody staining more sensitive and Culture of the
parasite most sensitive. for both parteners Metronidazole mg t.d.s. days, tinidazole gm single
dose. Condom limits transmission.
E. Treatment
F. Control
Hemoflagellates Leishmania Trypanosoma cruzi amastigote and promastigote Amastigote,
trypomastigote Trypanosoma brucei and epimastigote epimastigote and trypomastigote
Leishmania life cycle
A. Biology of Leishmania organisms
. . . . Organisms Old world cutaneous L.tropica, L. major New world cutaneous L mexicana
New world mucocutaneousL. braziliense. Visceral L. donovani, and L. infantum Final host
Man only in L.donovani and L. tropica. Man and animals in the others Habitat
Reticuloendothelial cells of skin or viscera. Exit diagnostic stage Amastigotes within
macrophages. Life cycle
B. Epidemiology of Leishmania infection
. Intermediate host vector phlebotomus old world and Lurzomyia new world. . Reservoir host
arboreal mammal monkeys New.World. Rodents in African donovani and L. major. Dogs in
L.infantum Transmission cycles Zoonotic in all except Indian L. donovani, and L. tropica. .
Infective stage Metacyclic promastigotes regurgitated from pharynx . Mode of infection
During vector feeding metacyclic promastigotes are regurgitated into the bite wound not in
the salivary gland
C. Hostparasite relationship
. Ulcerative cutaneous lesions self healing, painless, nonpruritic ulcer dry tropica wet major. .
Scaly non ulcerated lesions i. Anergic diffuse cutaneous L.mexicana and ethiopica with
abundant amstigotes . ii. Hypersensitive leishmaniasis recidivans L. tropica with rare
amstigotes. . Mucocutaneous lesion in of cutaneous leishmaniasis braziliense. . Visceral
leishmaniasis Kalaazar fever, anaemia, hepatosplenomegaly in L. donovani. . Post kalaazar
dermal leishmaniasis lesion that resembles leprosy. It occurs months or years after
successful treatment
D. Diagnosis of leishmaniasis
Cutaneous types Detecting amastigotes in the raised border of the lesion and positive
leishmanin skin test. Visceral type Detecting amastigotes in bone marrow, lymph nodes or
spleen aspirates and serotesting to detect o specific IgG anti K antigen antiIgG , Intradermal
leishmanin test is usually negative
E. Treatment
Pentostam mg/kg/d IM or IV for ds, Pentamidine mg/kg on alternate days for doses.
Amphotericin B parenteral and orally aminosidine paromomycin. Protective clothing, insect
repellents, insecticides and control of reservoirs.
F. Control
African trypanosomes Basic morphology and life cycle
Trypanosoma brucei
A. Biology
Two organisms Trypanosoma gambiense in West and T. rhodesiense in East Africa Final
host . Man and domestic animals for T. gambiense. . Game animals and sometimes man for
T. rhodesiense. Habitat Blood lymphatics CNS vessels. Exit diagnostic stage Blood stream
short stumby trypomastigotes Basic morphology and Life cycle
Trypanosoma brucei life cycle
B.Epidemiology
Distribution T. gambiense in rainforest, riverine and lakes in West Africa. T. rhodesiense in
dry bush and woodland in East africa Transmission Intermediate host vector o Glossina
palpalis in West and G morsitans in East. Infective stage metacyclic trypomastigotes in saliva
Mode of infection o Glossina injects saliva with metacyclic trypomastigotes into skin. o
Congenital transmission and o Accidental lab inoculation are recorded.
C. HostParasite relationship
. . . The parasite in skin Chancre swelling in the bite site The parasite in blood fever and
headache lymphadenopathy posterior cervical L.N. Winterbottom sign The parasite in CNS
anorexia amp apathy severe sleep disturbance. neurological signs delayed pain sensation
Kerandle sign. Coma and death.
D. Diagnosis
Detecting trypanosomes in blood, lymph nodes or spinal fluid CSF. o IgM in serum, CSF.
E. Treatment
Pre CNS o Pentamidine gambiense, or o suramin for rhodesiense amp gambiense CNS o
Melarsoprol. o Difluoromethyornithine DFMO.
F. Control
Treat cases and reduce the vector
American trypanosome Basic morphology and Life Lycle
American trypanosomes Trypanosoma cruzi
A. Biology
Final host Man and armadillo. Habitat Free trypomastigotes in blood low parasitaemia and
Intracellular amastigotes in spleen, liver, lymph nodes and muscles. Exit diagnostic stage o
Blood stream short stumpy trypomastigotes Basic morphology and Life cycle o o
Trypanosoma cruzi life cycle
B. Epidemiology
Distribution South and central America Transmission Intermediate host vector Kissing bugs
Triatoma via infected feces Reservoir hosts various mammals Transmission cycles sylvatic
and human cycles. Infective stage metacyclic trypomastogotes. Mode of infection . During
vector feeding metacyclic trypomastigotes are released into feces. They enter via the bite
wound near the mouth or the eyes. . Blood transfusion, . congenital, and . accidentally by
ingestion of contaminated food
C.HostParasite relationship
Pathogenesis is parasite mediated damage, or by autoimmunity. Acute stage . Chagoma
Rmana sign in the bite site periorbital edema and conjunctivitis few days postinfection and
persists for months. . Fever, malaise, lymphadenopathy and/or acute myocarditis for months.
Chronic stage o After decades of latency, it is manifested as cardiomyopathy and autonomic
neural dysfunction megaesophagus and megacolon.
D. Diagnosis
Detecting trypanosomes . In blood smear, . In buffy coat layer during the acute stage. . In
Culture NNN media. . By xenodiagnosis. . By PCR. Detection of specific serum IgG by Elisa
in chronic stage.
E. Treatment
o o o Acute stage Nifurtimox mg/kg/h Po for ds or Benznidazole . mg/kg/h for ds. Chronic
stage No specific drug in the chronic stage is useful. Treat symptoms.
F. Control
improve housing conditions. Insecticides. screening blood donors.
Life cycle of Plasmodium
Plasmodium species
. . . . Benign malaria Plasmodium vivax tertian malaria Plasmodium ovale. Oval tertian
malaria Plasmodium malariae quartan malaria malignant malaria Plasmodium falciparum
malignant sutertian malaria
.Final host Female Anopheles mosquitoes .Habitat in FH stomach lumen then stomach wall.
.Exit stage from FH Sporozoites. .Exit stage from IH man diagnostic ring, schizont and
gametocytes in all species except falciparum ring and gametocytes only.
A. Biology
B. Epidemiology
Distribution Tropical and subtropical areas. Formerly throughout temperate areas.
Transmission Intermediate host human. Commonly in liver cells and RBCs. Reservoir host
None except P. malariae monkeys.. Infective stage sporozoites in mosquitos saliva or
merozoites in RBCs. Mode of infection . mosquito injects sporozoites into blood vessels
percutaneously. . Transmission of merozoite in RBCs via blood
transfusion or transplacentally.
C. Hostparasite relationship
Clinical features
Fever cold, shivers hot up to oC sweating hypopyrexia sleep. Anemia due to hemolysis and
cytokine suppression on erythropoiesis severe in falciparum, Splenomegaly and
hypersplenism anemia. Jaundice due to massive and repeated hemolysis severe in
falciparum. Abortion, stillbirth in pregnant womenesp primigravidae infected with P
falciparum.
complications
Falciparum malaria .cerebral malaria and death .Persistent anaemia exists because
recrudescence of blood forms that survive the immune attacks .Algid malaria is characterized
by rapid development of shock due to sudden hypotension and fall of temperature.
.Blackwater fever It results from massive intravascular hemolysis and consequent
hemglobinuria.
Plasmodium vivax and ovale relapse up to years due to latent liver hynozoites. P. malariae
glomerulonephritis and nephrotic syndrome. P. vivax Splenic rupture is rare complication but
with high mortality . Hyperreactive malarial splenomegaly may develop with recurrent
infections.
D. Malaria diagnosis
.Light microscopy of thin and thick blood films to detect ring, schizont and gametocytes in all
species and only ring and gametocytes in falciparum species sensitive in field and specific
.Rapid diagnostic strip or cassette format tests based on pLDH OptiMal. sensitive. It
Differentiates flaciparum from others based on PfHRPII sensitive .Fluorescent microscopy
Acridin orange AO stained thick blood film sensitive and specific .Quantitaive buffy coat QBC
sensitive and gt specific
Differentiation of plasmodium sp
E. Treatment . Benign malaria Cloroquine base PO for days. If vivax/Ovale give primaquin for
days after chloroquine to treat liver stage and prevent relapse. . Falciparum malaria If can
swallow and has no complications, give quinine salt PO for d tetracycline, doxycyclin or
clindamycin for days. If seriously ill take to ITU give quinine IV. F. Control . Avoid the major
sources of infection mosquito. . Chemical prophylaxis chloroquine base or proguanil, PO.
Take drug one week before travel and continue for weeks after return.
Outline of Txoplasma life cycle
A. Biology of Toxoplasma
Final host Cats Habitat Intracellular in enteroepithelial cells of gut. Exit stage from FH
Immature oocyst. No exit stage from IH Basic morphology and Life cycle
B. Epidemiology of Toxoplasma
Distribution Worldwide. . Transmission Intermediate host mammals including human.
commonly in skeletal muscle, myocardium, and brain Reservoir host cats, rodents and
domestic animals. Infective stage mature oocysts, tissue cysts, tachyzoites. Mode of
infection .Ingestion of undercooked infected meat containing Toxoplasma cysts. .Ingestion of
the oocyst from fecally contaminated food .Organ transplantation or blood transfusion.
.Transplacental transmission. .Accidental inoculation of tachyzoites.
C. Hostparasite relationship
. Adymptomatic infection. . Fever and lymphadenopathy . . Encephalitis, acquired
retinochoroiditis or pneumonitis in the immune compromised. . Congenital toxoplasmosis .
abortion, stillbirth, hydrocephalus and/or congenital retinochoroiditis. The latter may manifest
early or later up to years after birth.
D.Diagnosis of toxoplasmosis
Observation of parasites in LN biopsy. Isolation of parasites from blood BCL by
intraperitoneal inoculation into mice. Detection of parasite genetic material by PCR, in
congenital infections in utero. Serologic testing Acute infection is confirmed by by a fold rise
in specific IgG antibody titer over weeks. IFA, ISAGA, IHAT and ELISA are the routine
methods of diagnosis to detect specific IgM, IgG, IgE and IgA.
Immunofluorescent antibody test IFA
Positive test Negative test
E.Treatment
Often none is used except in . If the eye is involved or in the immunecompromized
Pyrimethamine Daraprim for weeks, sulfadiazine. . Women with seroconversion during
pregnancy spiramycin g/h daily for days.
F.Control
Avoid the two major sources of infection raw meat and cont. cat feces.
Outline of Cryptosporidium life cycle
A.
Biology of Cryptosporidium
species hominis and parvum Final host man and cattle Habitat intracellular extracytoplasmic
within the brush borders of the enterocytes of whole GIT, biliary and respiratory epithelia. Exit
diagnostic stage mature Oocyst asporocystic tetrazoic in human and calves feces. Basic
morphology and Life cycle
B. Epidemiology of Cryptosporidium
Distribution About of the adult population in developed counties and in developing C.
Transmission . Intermediate host no. . Reservoir host cattle in C parvum. No reservoir host in
C. hominis. . Infective stage Oocyst. . Mode of infection Humantohuman fecaloral
transmission. Animaltoperson transmission. Waterborne transmission
C. Hostparasite relationship
Incubation period of days The patient develops watery diarrhea, This may be associated
with abdominal cramps and a lowgrade fever Stool microscopy Modified acidfast staining of
stool shows redstained round oocysts against a bluegreen background. Antigendetection
assays are more sensitive and include IFA assays, ELISA, and IC tests. Polymerase chain
reaction PCR assays, more sensitive than others.
D. Diagnosis of cryptosporidiosis
E. Treatment Nitazoxanide Cryptonaz. For days with food F. Control Using a home
microstraining water filter, to remove particles m in size.