c HEMATOLOGY CORRELATES (Practical Exam Reviewer) BLOCK XVIII

Felice Garingalao-Molina, M.D., FPCP, FPASMAP SUBJECT Micro-Para

December 17, 2015 LECTURE Laboratory

HABITAT (REVIEW)
1. Small Intestines: CASH
Capillaria
Ascaris
Strongyloides
Hookworm
2. Large Intestines:
Trichuris
Enterobius
3. Extraintestinal
Lymph nodes and lymph vessels: Brugia, Wuchereria
Eyes and meninges: Angiostrongylus
Muscles: Trichinella
Microorganism
1. Trichuris Trichiura Male
Soil Transmitted Helmints
CN: Whipworm
Lifespan: 2 years
Habitat: Cecum
Disease: Trichuriasis,
Trichocepaliasis, Whipworm
Infection
MOT: Ingestion of eggs,
Infective Stage: Embryonated
Eggs
Treatment: Mebendazole
Male: Coiled posterior with a
single spicule and refractile
sheath
NEMATODES
Mode of Transmission:
1. Ingestion Most common
Embryonated eggs- Enterobius, Ascaris, Trichuris (E-A-T egg)
Infective Larvae Capillaria (fish), Angiostrongylus (snail), Trichinella (pork)
2. Skin Penetration Hookworm, Strongyloides
3. Bite of Mosquito Vectors Wuchereria, brugia
4. Autoinfection Strongyloides, Enterobius, Capillaria
5. Inhalation Enterobius, Ascaris
Slide Clinical Manifestations Diagnosis/Laboratory
Findings
Actual Slide: Petechial hemorrhages in the intestinal mucosa due to the Direct fecal smear (DFS)
anterior portion of the worm embedded therein and may Kato thick Smear-Useful
predispose to amoebic dysentery for mass examination
Rectal prolapse Kato Katz : for egg
Appendicitis or granuloma due to inflammation and irritation counting to determine
caused by the worms on the appendiceal lumen cure rate, ERR (Egg
No lung pathology reduction Rate) and
Asymptomatic: light infection intensity of infection
Symptomatic: >50,000/g
Severe diarrhea of dysentery syndrome: >20,000/g:
Heavy parasitism: worms may be seen all throughout the large
bowel
o blood streaked diarrheal stools
Internet Source:
o abdominal pain and tenderness
o nausea
o vomiting
o Anemia (if heavily parasitized)
o weight loss

Page 1 of 8
Female: Bluntly rounded
posterior ends
Egg: Lemon shaped with a
plug-like translucent polar
prominences, Yellow Outer
and Transparent inner shell
2. Hookworm Ova
Ancylostoma duodenale,
Necator americanus
Habitat: Small intestines
Infective stage: Filariform
larva
Soil-transmitted helminth
Blood-sucking, attaches to
the mucosa of habitat
Usually seen in tropical or
subtropical areas as a single
or mixed infection
Usually chronic
Mild unlike ascariasis
Necator Americanus:
Buccal capsule has a ventral
pair of semilunar cutting
plates
Head is curved opposite the
curvature of the body
Ancylostoma Duodenale
Slightly larger than N.
americanus
Single-paired male and
female reproductive organs
Head continues on the same
direction as the body
curvature
Actual Slide
Internet Source:
(Ova) Bluntly rounded eggs,
single thin, transparent shell,
unsegmented at oviposition
(Filariform larva)
Clinical features: Final diagnosis depends
Mostly asymptomatic on finding hookworm
Pruritic maculopapular dermatitis (ground itch) eggs in feces: Parasite
Transient pneumonitis occasionally in different stages of
GI pain, diarrhea with eosinophilia development:
Iron-deficiency anemia (IDA): major consequence of chronic (Rhabditiform is
infection, hypoproteinemia weakness, shortness of breath diagnostic)
and skin depigmentation
Blood Studies:
Microcytic,
hypochromic anemia;
Hypoalbuminemia
DFS may not detect
parasites of egg count
is <400/g feces
Kato technique
Kato-katz method
Concentration
methods
Ex. Zinc sulphate
(ZnSO4) centrifugal
flotation and Formalin-
ether
o Increase positive
findings significantly
o Recommended
- Culture methods
Ex. Harada- Mori allow
hatching of larvae from
Left: Ancylostoma duodenale
eggs
Right: Necator americanus
 Buccal capsule has 2 pairs of
curved ventral teeth
3.Trichinella Spiralis Larva
CN: Pork Worm
Disease: Trichinosis
MOT: Ingestion of
undercooked meat
Infective Stage: Encysted
Larvae
Hosts: Different animal hosts:
Mostly mammals
4. Strongyloides Stercolaris
Filariform Larva
Free-living rhabditiform and
parasitic filariform stages
Disease: Stronglyloidiasis,
Cochin-China Diarrhea
Permits AUTOINFECTION
Infective Stage: Filariform
Larva
o Identification of
filariform larvae
o Studies: usually N.
americanus
Actual Slide Clinical symptoms arise from successive phases of: Diagnosis is usually
Parasitic enteric invasion, made based on clinical
Larval migration, and symptoms, and is
Muscle encystment confirmed by serology
o Asymptomatic: <10 larvae/g of muscle; or identification of
o May be life threatening: >50 larvae/g of muscle; encysted or non-
Marked local and systemic hypersensitivity reaction to encysted larvae in
encysted larva with fever and hypereosinophilia biopsy or autopsy
Periorbital and facial edema specimens.
Hemorrhages subconjunctivae, retina, nail beds (splinter
hemorrhages) Blood eosinophilia in
Splinter hemorrhages can also be seen in IE, but IE has a 90% of symptomatic
murmur, predisposing conditions cases
Internet Source: Myocarditis with tachyarrhythmias or heart failure
Fever up to 38.5C Elevated serum IgE
Irritating non-productive cough Elevated creatinine
Burning substernal discomfort aggravated by cough and deep phosphokinase (CPK)
inspiration Rise in parasite-
Chest x-rays: transient or intermittent small round or oval specific antibodies
infiltrates (eosinophilic pneumonitis) Surgical biopsy
Abdominal pain, small bowel obstruction
Loefflers syndrome (Pulmonary Eosinophilia)
Transient pulmonary lesions
Benign clinical course
Actual Slide: Three phases of infection: Clue: unexplained
1. Invasion of the skin by filariform larvae erythema, eosinophilia
pruritic, hemorrhagic papules Repeated
2. Migration of larvae through the body lobar pneumonia concentration
with hemorrhages techniques:
3. Penetration of the intestinal mucosa by adult female Harada-Mori culture
worms (may occur together to cause hyperinfection) practical, low cost for
Light infection: no intestinal symptoms mass screening
Moderate infection: diarrhea-constipation Baermann funnel
Internet: Baeles string test
 MOT: Skin penetration,
autoinfection (more fecally
transmitted than soil-
transmitted helminth)
Habitat: Small intestines
(duodenum and upper
jejunum) but may be all
throughout the alimentary
tract.
1. Diphyllobothrium latum
ova and Gravid Segment
CN: Broad Fish Tapeworm
Disease: Diphyllobothriasis
Infective stage: Plerocercoid
larva or Sparganum
First Intermediate Host:
Copepod
Second Intermediate Host:
Fish (ex. Minnow, small
freshwater fish)
Definitive host: Man, dog, cat,
etc.(Plerocercoid attaches to
the mucosal wall,matures in 3
weeks.
Adult:
Spatulate scolex, 2 bothria
or sucking grooves
Long neck
Mature proglottids 2-4 mm
long, 10-12 mm wide with
one set of reproductive
organs
Proglottids disintegrate only
when reproductive function
is completed
Eggs:
Heavy infection: intractable, painless, intermittent watery
and bloody diarrhea (Cochin-China diarrhea)
Some Complications:
o edema
o emaciation
o loss of appetite
o anemia
o lobar pneumonia
o malabsorption leading to cachexia
CESTODES
Actual Slide (OVA) Actual Slide (Gravid Segment) Infections are usually limited
to one worm
Symptomatic due to absorbed
toxins or by byproducts of
degenerating proglottids or
mucosal irritation
Hyperchromic, megaloblastic
anemia (defects in
maturation) with
thrombocytopenia and
leukopenia
Anemia similar to pernicious
anemia (bothriocephalus
anemia)
Jejunum: competition with
the host for cobalamin
(content is 50x that of T.
saginata)
With treatment, worms are
pushed down the intestines;
anemia is relieved
Internet:
Internet:
Duodenal aspiration
Small bowel biopsy
Disseminated
infection: sputum,
urine
Serology but may cross
react with filarial
History of residence or
travel to endemic areas,
raw fish diet
Lab: Pernicious type of
anemia (to differentiate
it from Diphyllobotriasis
examination of gastric
juice free HCl is useful)
PA- achlorhydia
Definitive diagnosis:
Fecalysis (kato
technique)
Characteristic:
operculated eggs,
proglottids, scolex
 Yellowish brown, moderately
thick shell, inconspicuous
operculum, small knob-like
opening
1. Paragonimus Westermani
Ova
MOT: Eating raw or
insufficiently cooked and
infected Sundathelpusa crabs
Common in Sorsogon
(Southern Luzon area)
Pathogenesis is mostly in the
lungs
Infective Stage: Metacercaria
Egg: Oval, yellowish, brown,
thick shelled. Has flattened
but prominent operculum.
First Intermediate Host:
Antemelania asperata and
Antemelania dactylus (snails)
Seccond Intermediate Host:
Mountain Crab
(Sudenthelphusa philippina)
1.Plasmodium falciparum
gametocyte
Protozoan, Pigment
Producing, Ameboid
Most common definitive
Host: Anopheles minimus
flavirostri. Can also be hosted
by A. litralis, A. maculates, A.
mangyanus
Disease: Malaria
TREMATODES
Actual Slide Differentials: Pulmonary. TB, bronchiectasis, lung abscess, pleural Radiographs
effusion -May aid in diagnosis but
difficult to differentiate
Chief Complaint: Cough, hemoptysis, difficulty of breathing paragonimiasis from PTB
In the lungs, paragonimus worms provoke granulomatous reaction, Definitive Diagnosis
gradually proceeding to development of fibrotic encapsulation. Detection of eggs in
Within the cyst, is blood-tinged purulent material containing eggs. sputum or stool; less
Early stages are asymptomatic frequently in aspirated
Internet Source: Dry cough, later producing blood stained or rust colored material from abscess or
sputum with foul fish odor, most pronounced in the morning pleural effusion
Chest pains, dyspnea, hemoptysis Paragonimiasis
Low grade fever, fatigue, generalized myalgia Antigen Intradermal
Chronic cough Skin test screening
Cerebral involvement-most serious complication, causing process, cannot
Jacksonian epilepsy, cerebral hemorrhage, edema, visual differentiate past and
disturbances, meningitis. present infections
Clinical symptoms are less severe after five to six years, Serology diagnosis
although worms are known to persist longer of extrapulmonary
Prognosis with light infections is good. Prognosis unfavorable in paragonimiasis
heavy infections and with cerebral involvement.
PROTOZOAN
Actual Slide: Pathological Process in the ERYTHROCYTE CYCLE Labs: leucocytosis,
coagulopathy,
P falciparum merozoites reduce RBC deformability due to the thrombocytopenia,
rigidity of the parasite, changes in the RBC exoskeleton, increase prolonged ProTim/
in membrane stiffness and cytoplasmic viscosity. RBC easily aPTT, decreased
ruptures fibrinogen
RBC altered membrane transport soluble antigens of P.
falciparum are potent inducers of pro/anti-inflammatory
cytokines form monocytes and macrophages
In P. falciparum, there is severe normocytic normochromic
anemia, bleeding, DIC, hemoglobinuria (black, brown, red)

Asexual Cycle:
Occurs in man, the vertebrate
and intermediate Host
Schizogony Merozoites
Gametogony Gametocytes
Sexual Cycle:
Anopheles mosquito, the
invertebrate and definitive
host
Sporogony sporozoites
Higly endemic in Palawan,
Kalingaa, Apayao, Agusan del
sur, Ifugao. MDR malaria can
be found in Davao del Norte,
Campostela Valley, Palawan
2. Entamoeba Histolytica
(No actual slide for this)
Infective Stage: Non invasisve
infection: Cysts, Invasive
Infection: Trophozoites
Transmission: Transmission
occurs via the faecaloral
route,.
Pseudopod-forming
nonflagellated protozoan
parasite, for movement
Most invasive of the
entamoebidae family
P. malariae has the longest erythrocytic cycle
In P. falciparum, only ring form can be seen in microscope for
diagnostic purpose. Occasionally, you will see gametocytes that
are banana-shaped
CLINICAL:
MALARIA
Considered the most important parasitic disease affecting man
transmitted by the bite of infected Anopheles mosquito
P. falciparum (70% of cases)
P. vivax (<30%)
P. ovale
P. malariae (1%)
P.knowlesi (initially there is only animal-to-animal
transmission, but now, it is known that it can be
transmitted to humans)
It depends on the species when it comes to invasion. P.
falciparum can invade young and old RBCs, so only this species
can manifest severely. P. malariae prefers old RBCs
Internet Source:
Internet Sources: The clinical spectrum ranges from asymptomatic infection, It can be diagnosed
diarrhoea and dysentery to fulminant colitis and peritonitis as by stool samples, but
well as extraintestinal amoebiasis. it is important to
note that certain
Acute amoebiasis can present as diarrhoea or dysentery with other species are
frequent, small and often bloody stools. Chronic amoebiasis can impossible to
present with gastrointestinal symptoms plus fatigue, weight loss distinguish by
and occasional fever. Extraintestinal amoebiasis can occur if the microscopy alone.
parasite spreads to other organs, most commonly the liver where Trophozoites may be
it causes amoebic liver abscess. Amoebic liver abscess presents seen in a fresh fecal
with fever and right upper quadrant abdominal pain. smear and cysts in
an ordinary stool
sample. ELISA or RIA
can also be used.
 OTHER CAUSATIVE AGENTS

Schistosoma japunicum (fluke) Schistosoma Japonicum Ova Microfilariae of Wuchereria Leptospira interrogans
bancrofti

Staphylococcus epidermidis Streptococcus pneumoniae DengueVirus

Ebola Virus
ATLAS SOURCES ( Supplemental Study according to Maam Eden)

Ring Forms of P. Falcifarum.The ring Schizont of P. falcifarum.

forms are 1.5um in diameter and
multiple infection of RBC is commom.
They often show double chromatin
dots and parasitized red cells are not
enlarged and may contain Maurers
Ring Forms of Plasmodium falcifarum
dot( but not seen here).
Usually not found in the peripheral
circulation, but they are showm in
the final stage of severe infection.The
mature schizont form 18 to 24 Macrogametocyte of P. Falciparum
merozoites.
 P. Falciparum.The female
gametocyte is cresentic or banana
shaped and is called crescent.
Cytoplasm is stained blue and
nucleus red by Giemsa Stain.
Liver of an autopsy case of falcifarum
malaria infection. 37 year old man,
infected and onset began in Africa;
then he was sent back to Japan.
Diagnosis was not established until
shortly before death.Liver is
enlarged.
The male gametocyte is less pointed
and stains more lightly than the
female gametocyte
Section of the liver.Degenaetaion of
hepatic cells and malarial pigment in
Kupffers cells are seen.
P. Falciparum. Thick blood Smear Micogametocyte of P. Falciparum
with Giemsa Stain
Spleen of an autopsy case of
falcifarum malaria infection. Marked
Section of the spleen. The presence of
splenomegaly is seen and parasite
malarial pigment is present.
density in peripheral blood shortly
before death was 9x105 /mm3