Parasitology
Dr Hussien Bamashmous
PROTOZOA
OR
METAZOA
PROTOZOA
Protos : first Zoon : animal
Phylum of animal kingdom which includes simplest animals
most are unicellular
some are colonial
REPROPDUCTION:
usually asexual by fission
some sexual reproduction
EXAMPLES OF PROTOZOAL DISEASE:
Malaria
Amebiasis
Giardiasis
Trichomoniasis
Toxoplasmosis
Visceral leishmaniasis
Pneumocystis carinii
METAZOA
META: after / beyond ZOON: animal
DIVISION OF THE ANIMAL KINGDOM THAT INCLUDES
ALL “MULTICELLULAR FORM”
They are either
NEMATODES or CESTODES
1- NEMATODES
NEMA: thread EIDOS: form
Nematohelminthes are either :
round, cylindrical, spindle shaped.
Examples:
ENTEROBIASIS = OXYURIASIS ( pin worm)
ASCARASIS = round worm
ANCYLOSTOMIASIS = hook worm
TRICHINOSIS
TRICHURIASIS = whip worm
2- CESTODES
KESTOS : GIRDLE
Subclass of Cestoidae phylum =
“PLATYHELMINTHES”
EXAMPLES:
TAENIASIS: tapeworms = scolex + segments
(proglottidis)
VISCERAL LAVAR MIGRANS
FILARIASIS
BILHARSIASIS (schistosomiasis)
MALARIA
mal - aria
MALARIA
ESSENTIALS OF DIAGNOSIS:
Residence in or travel to an endemic area
High fever, chills, headache
Jaundice, vomiting, diarrhea
Anemia, splenomegally
Seizures, coma
Malaria parasite in the blood smear
GENERAL CONSIDERATIONS:
Malaria kills 1,000,000 children/ year
Resurgence is observed now
Female Anopheline mosquito transmits the
parasite:
Plasmodium Vivax (most common)
P. Falciparum (most virulent)
P. Ovale (similar to Vivax)
P. Malariae
LIFE CYCLE:
INFECTED HUMAN BLOOD (GAMETOCYTES)
Sucked by Anopheline mosquito
In its stomach wall
OOKINTE OOCYST MATURE OOCYST
rupture SPORPZOITE
to its salivary glands bite uninfected person
In the uninfected person Sporozoites disappear within
1/2 hour from the circulation and infect the hepatocytes
HEPATIC PHASE: ( PRE-ERYTHROCYTIC PHASE)
about 2 weeks for all
3-5 weeks for P. Malarie
Hypnozoites ONLY FOR P.VIVAX AND OVALE
which is responsible for future relapses.
Merozoites leave the liver thereafter to infect the
RED BLOOD CELLS ERYTHROCYTIC CYCLE
ERYTHROCYTIC CYCLE (ASXETUAL CYCLE)
ERYTHROCYTE HAEMOLYSIS
METROZOITES TROPHOZOITES SCHIZONTS
METROZOITES (which will be released by heamolysis)
SYMPTOMS
IMMATURE GAMETOCYTES
MATURE GAMETOCYTS (male & female)
Sucked by mosquito
REPEAT THE CYCLE
P. VIVAX affects young red cells
ruptures symptoms X 48 hours
P. MALARIAE old red cells symptoms X
72 hours
P. FALCIPARUM all cells NO
CLASSICAL TRIAD OF SYMPTOMS
SURVIVAL (especially in endemic area)
immunity
intensity of the cycles
NO HEPATIC PHASE (pre- erythrocytic phase) with:
1. Blood transfusion
2. Needle stick
3. Congenital malaria
Susceptibility varies genetically
Partial resistance to infection with :
1. Hemoglobin S
2. Hemoglobin F
3. Thalassemia
4. G6PD deficiency
Maternal immunity protects the neonate despite placental infection
Clinical findings varies according to :
1. strain
2. host immunity
PRESENTATION:
CLASSICAL TRIAD WITH P. VIVAX & P. OVALE
COLD STAGE
AFTER ½ HOUR HOT STAGE
AFTER 1-6 HOURS SWEATING
OTHER SYMPTOMS AND SIGNS:
Pallor and irritability
Poor feeding
Vomiting and diarrhea
Jaundice
Splenomegally
Hepatomegally
OLDER CHILDREN:
Headache and backache
Myalgia
Fatigue
IF UNTREATED RELAPSES STOPPED:
Within a year with P. Falciparum
Within several years with P. Vivax
May occur decades later with P. Malariae
INFECTION DURING PREGNANCY:
Intrauterine growth retardation
Preterm
Congenital malaria
LABORATORY FINDINGS:
Multiple thick smears Giemsa stain
Thin smear Wright stain
In P. falciparum only ring form of
Trophozoited & Gametocytes are seen in
peripheral smear.
GAMETOCYTES MAY PERSIST FOR DAYS
FOLLOWING ADEQUATE THERAPY
Complete Blood Count:
Normocytic normochromic anemia
Leucopenia, leucoytosis
Normal or low platelet count
High retics
LFT:
indirect and direct hyperbilirubinaemia
mild transaminase elevation
hypergammaglobinaemia
Occasionally:
low complement
positive rheumatoid factor
positive ANA
false positive VDRL
Differential diagnosis:
TUBERCLUSIS
BRUCELLOSIS
BORRELOSIS
SQUENTIAL COMMON INFECTIONS
HODGKEN’S DISEASE
JUVENILE RHEUMATOID ARTHERITIS
RAT BITE FEVER
CAT-SCRATCH FEVER
IDIOPATHIC PERIODIC FEVER
TYPHOID FEVER
MYCOPLASA PNEUMONIA
COMPLICATIONS AND SEQUALAE:
CHRONIC MALARIA SPECIALLY P. FALCIPARUM
Anemia
Deblitation
Massive Splenomegaly (tropical splenomegally syndrome)
MICROTHROMBOSIS AND ISCHAMIA
Intestinal Tract bleeding and diarrhea
Lung pneumonitis
Brain diffuse edema, seizures, encephalopathy
INTRAVASCULAR HAEMOLYSIS
hemoglobinuria renal failure ( black water fever)
CHRONIC P. MALARIAE
nephrotic syndrome
PREVENTION
SPOROZOITES resistant to drugs
CASUAL PROPHYLAXIS = drugs which act on hepatic
phase
SUPPRESSION = drugs which act on erythrocytic phase
CHLOROQUINE = safe in pregnancy
CHLOROQUINE RESISTENCE ALL OVER EXCEPT:
Central America
Haiti
Panama
Egypt
Most of the middle east
IN RESISTENT-FREE AREA:
Cholorquine 5 m/kg of base max. 300 mg once/week.
ONE WEEK BEFORE TRAVEL & FOUR WEEKS
AFTER RETURN
IN CHLOROQUINE RESISTENT AREA:
Mefloquine (not if wt. is less than 15 kg)
Maloprim = pyrimethamine + Dapsone
Fansidar = pyrimethamine + Sulfdoxane
FOR P.VIVAX & P. OVALE
2 week course of primaquine phosphate
SCREEN FOR G6PD BEFORE PRIMAQUINE
INSECT REPELLENTS & MOSQUITO NETTING (night)
TREATMENT:
New drugs has been discovered in the treatment
of Malaria .
They are called the (ARTEMESSININS).
They are derived from a Chinese plant.
Introduced in the market since 1996.
They act as internal bomb inside the Malaria
parasite using its own hydrogen peroxide.
The best treatment is called ACT.
ACT : is combination of
ARTEMESSININS and CHLOROQUINE.
Unfortunately in the markets now in many
countries there are mal-manufactured drugs with
poor effectiveness and possibly emerging
resistance.
Cont. TREATMENT:
CHLOROQUINE PHOSPHATE Drug of choice for :
Nonresistant P.Falciparum
Most infections by other species
Course of “3 days” ERADICATES THE ERYTHROCYTIC
PHASE
Give orally: 10m/kg (max 600mg) as initial dose
5 mg/kg 6 hours, 24 hrs & 48 hrs later
MEFLOQUINE
effective but has neuropsychiatric side effects
QUINIDINE GLUCONATE (parental)
10-14 mcg/kg as a loading dose
then 0.02 mg/kg/min
CHLOROQUINE RESISTENCE MALARIA:
(P.O.)
QUININE SULPHATE x 3 days + PYRIMETHAMINE x 3
days + SULPHADIAZINE x 3 days
QUININE SULFATE x 3 days + TETRACYCLINE x 7
days
(Parentral)
QUININE DIHYDROCHLORIDE
QUININE GLUCONATE
GENERAL MEASURES:
Hydration and fever control
Blood and needle precautions
Hospitalization with:
persistent vomiting
severely ill
Non-immune to P. Falciparum
Iron and folate level
Hepatitis and HIV screening (especially for drug
users)
FOR CELEBRAL MALARIA:
Rule out other causes
Anticonvulsants
Parental antimalarial
Control of cerebral edema
Disferoxamine
Steroids = Contraindicated ( except with
intravascular hemolysis)
Giardiasis
Essentials of diagnosis
Chronic relapsing diarrhea
Flatulence, bloating, anorexia, poor wt. gain
Absence of fever and blood in stool
Presence of “TROPHOZOITES” in diarrhe or stool
Cysts in formed stools
GENERAL CONSIDERATIONS:
In many areas = most common protozoan in children
Caused by “GIARDIA INTESTINALS’’
Water Drinking (contaminated water) in endemic areas
Food-borne outbreaks do occur
Incidence in “ DAYCARE NURSERIES” up to 50%
Incidence in mental instituations
The parasite resides in the duodenum and jujenum
Inflamation & subtotal villous atrophy
Clinical findings
Cyst ingestion trophozoites live non-
invasively in the small intestine
Symptoms develop in 1-3 weeks
Diarrhea (soft)
Steatorrhea = mucus but no RBC / WBC
Abdominal cramps
anorexia, vomiting wt. lost
The illness may last days to months or my relapse
Laboratory findings
CBC= normal (no eosinophils)
Fresh stool = +ve trophozoites
Formed stool = oval cysts
Duodenal aspirate & biopsy
String test (Enterotest)
Giardia antigen in stool
Differential diagnosis
Toddler’s diarrhea
TB enteritis
Chronic amoebiasis
Other causes of steatorrhea.
PREVENTION:
Avoid unclean water and food stuffs
Hand-washing is important
Animals are not vectors
Asymptomatic carrier identify and treat if
needed
Treatment
Treat symptomatic day care center cases & their
contacts
Drugs
Furazolidine: 2mg/kg X 6h X 7-10 days
Metronidazole: 5m/kg X 8h X 5-10 days
Quinacrine HCL: 2mg/kg X 8h X 5-10
days
NB. giardiasis maybe self limiting and may relapse
Leshmaniasis
General consideration
Caused by protozoan of the genus
“leishmania”
Conveyed by female sand fly in which
flagellate (proamistigote) develop
In man in monocytes and macrophages
amastigotes (leishmann-donovan
bodies)
Visceral leishmaniasis (kala azar)
In India man is the main host
In Mediterranean dogs and foxes are main
reservoirs
Transmission by: sandflies
blood transfusion
Multiplication by simple fission in monocytes &
macrophages in various organs huge
hepatosplenomegally and lymphadenopathy
Lishmania Malnutrition and Immune
Suppression Intercurrent infections
Tuberculosis
Clinical presentation
Incubation period = 1-2 months up to 10 years
Insidious onset of fever
Temperature is either remittent or intermittent
Hepatosplenomegally
Lymphadenopathy
If untreated severe anemia and wasting
Facial hyperpigmentation
After therapy: Dermal leshmaniasis,
Hypopigmentaed macules,
Erythematous macules,
Nodular eruption
Diagnosis
Pancytopenia: bone marrow suppression +
hypersplenism
Immunoglobulin (esp IgG) & albumin
Aspirated and cultures from
Bone marrow,
liver & spleen,
lymph nodes
+ve Serology : immunoflourescene
C.F.T
Leishmania skin test negative
using killed proamstigotes
Differential diagnosis
Infective endocarditis
Typhoid fever
Brucellosis and tuberculosis
Lymphomas
Bilharizaisis
Malaria
Treatment
Asia (India) good recovery
Sudan & east Africa more resistant
Drugs used
sodium stibogluconate
pentavalent antimony compound
IM or IV for 10 days,
could be repeated after 10 days if needed
days
In resistant cases use:
Pentamidine Isethionate
2 hydroxy Stilbamidine
Amphotericin B
Prevention:
In endemic areas destroy stray dogs and
foxes
Sandflies should be combated by insecticides
& repellents
No vaccine available
Other types of leishmaniasis
Leishmania of old world = LESHMANIA
TROPICA (ORIENTAL SORE)
Geographical region
Asia, India, North Africa, Arabia
Vector: sandfly,
transmits the parasite from animal to man (ZOONOSIS)
symptoms and signs
incubation period 2-5 weeks up to years
papule at the bite site (usually the face and limbs)
ulceration of the papule scarring
Diagnosis
Dry needle aspirate or skin slit smear +ve
for the organism
Positive skin test
Positive serology
Therapy
antimony compound reduces the
scarring
Resistant cases: pentamidine +
amphotericin
There is a vaccine for L.Tropica
Leishmania of the new world
Leishmania Brazilliensis Espundia
Leishmania Mexicana Chicleroulcer
Leishmania peruviana Uta
Geographical distribution: south america
Vector: sandfly
Symptoms and signs:
Painful mucocutaneous ulcers or granulomas
Nasolabial lesions (common)
Lips, palate
terrible suffering and disfigurment
Diagnosis:
skin biopsy
+ve skin test
serology
Therapy
Antimony compound
Establishing espundia Amphotericin
Brucellosis
IT IS A ZOONOTIC DISEASE CAUSED BY
SPECIES BRUCELLA:
1. Brucella Melitensis = goats and sheep
2. Brucella Abortus = cattle
3. Brucella Suis = swine
4. Brucella Canis = dogs
Routes of infection in pediatrics:
Direct contact
Inhalation of aerosols
Ingestion of raw milk or milk products from infected
animals
Incidence could be decreased by:
Control of the disease in domestic animals
Pasteurization of milk
Presentation in Children:
50% acute disease
Other 50% subacute disease
Eitiology:
Brucella named for SIR DAVID BRUCE who first isolated
the organism in 1887
Epidemiology
In industrialized countries occupational hazard
In USA pediatric cases about 10%
In Arabia more
Endemic brucellosis
caused by ingestion or raw milk, cream, butter,
cheese or ice cream
Organism my directly invade: Eye, nasopharynx and
genital tract
Brucella can survive up to 3 weeks in refregerated
garcass
Endemic disease is maintained “In Animals” through
excretion of large numbers of the organisms:
in genital secretions and milk with vertical and horizontal
transmission
Brucella causes abortion in Animals
Human to human transmission is Rare
but may be caused by:
1. Blood transmission
2. Bone marrow transplantation
3. Transplacental
4. Perinatal exposure
Pathology and pathogenesis
BRUCELLAE facultative intradellular parasite
Capable of surviving and multiplying within phagocytes, red
blood cells and many cell lines
Nonspecific host factors triggered
Agglutinins
Polymorphs
Complements
Opsonization & phagocytosis But Intracellular
Killing Is Less Effective
multiplications of the organism induction of immunity
Host responds by forming:
1. Specific antibodies
IgM appears within 1 week and comes down by 3
months
IgG appears by 2-3 weeks and persists if
untreated or partially treated
2. Others like:
agglutinins
opsonins
precepitins
C.F. antibodies
Brucella Variants are:
S. varient (smooth): more virulent
resist intraleukocyte killing
R. Varient (hard) : less resistant
All species of brucella produce
Granuloma in the liver, spleen, l.nodes, bone marrow
Granulomoatous inflammation of gall bladder
Interstitial orchitis
Endocarditis with vegetation
Granuloma in myocardium
Involvement of : brain (neruobrucellosis),
skin,
bone
Clinical manifestations:
Non specific: Fever,
Arthralgia and arthritis,
Malaise,
Weakness,
Neurobrucellosis Depression
Incubation period: Few Days to Months
The interval between onset of the Symptoms
and Diagnosis =150 days (mean of 4 weeks
Hepatosplenomegaly 30-40%
Uncommon manifestations
Osteomeyelitis (non-suppurative)
Myocarditis
Endocarditis
Genitourinary
Neonatal brucellosis
Diagnosis:
History
Examination
Investigations
CBC = hemolysis,
pancytopenia (hypersplenism)
Bone marrow = involvement with haemophagocytosis
reported
Acute disease before treatment:
Blood cultures = +ve up to 50%
Bone marrow cultures= +ve up to 90%
Serology (IgM & IgG)
- high titred serum = prozone
- Inhibition dilute with sera
Successful treatment
Rapid decline of IgM
IgG titer may persist for months or years
High IgG titer persistent infection of relapse
More sensitive test = enzyme immuno assay
Tissue biopsy (liver)
Differential diagnosis:
Acute brucllosis
Influenza
Typhoid fever
Infectious mononucleosis
Tuberculosis
Tularaemia
Persistent brucellosis
Malignant histocycosis
Lymphomas
Tuberculosis
Prevention:
Immunization of domestic herds
Pasteurization of milk
Periodic assessment of animals (slaughtering
infected ones)
Hunters should use caution in handling
potentially infected animals
Treatment:
Treatment of choice is “TETRACYCLINE” in
combination :
Doxycyline (orally)
5 mg/kg/day max 200m/day in 2 divided doses
+(Plus)
Streptomycin (IM)
30 mg/kg/day divided every 12 hours
OR
Gentamicin (IV)
5 - 7.5 mg/kg/day divided every 8 hours8h
For Children:
Trimethoprim – sulfamethoxazole (orally )
10 - 12 mg/kg/day (Trimethoprim)
+(Plus)
Rifampacin
15 - 20 mg/kg/day
( Duration of treatment = 3 - 6 weeks )
Delay in Diagnosis:
High antigen load after treatment
JARISH - HERXHEIMER like reaction Treated
with Steroids if needed
Prognosis:
Untreated cases case fatality rate is 3%
Most deaths are due to specific organ involvement (as
Endocarditis)
Following treatment excellent prognosis
Delayed diagnosis prolonged course
Complete recovery may take up to 6 months
Re-infection is uncommon
Immune individuals if invadertently injected with the cattle
vaccine local and mild systemic disease