c HEMATOLOGY CORRELATES (Practical Exam Reviewer) BLOCK XVIII

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

December 17, 2015 LECTURE Laboratory

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

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Female: Bluntly rounded
posterior ends

Egg: Lemon shaped with a

plug-like translucent polar
prominences, Yellow Outer
and Transparent inner shell
2. Hookworm Ova Actual Slide Clinical features: Final diagnosis depends
Mostly asymptomatic on finding hookworm
Ancylostoma duodenale, Pruritic maculopapular dermatitis (ground itch) eggs in feces: Parasite
Necator americanus Transient pneumonitis occasionally in different stages of
GI pain, diarrhea with eosinophilia development:
Habitat: Small intestines Iron-deficiency anemia (IDA): major consequence of chronic (Rhabditiform is
Infective stage: Filariform infection, hypoproteinemia weakness, shortness of breath diagnostic)
larva and skin depigmentation
Soil-transmitted helminth Blood Studies:
Blood-sucking, attaches to Internet Source: Microcytic,
the mucosa of habitat hypochromic anemia;
Usually seen in tropical or Hypoalbuminemia
subtropical areas as a single
or mixed infection DFS may not detect
Usually chronic parasites of egg count
Mild unlike ascariasis is <400/g feces
Kato technique
Necator Americanus: Kato-katz method
Buccal capsule has a ventral Concentration
pair of semilunar cutting (Ova) Bluntly rounded eggs, methods
plates single thin, transparent shell, Ex. Zinc sulphate
Head is curved opposite the unsegmented at oviposition (ZnSO4) centrifugal
curvature of the body flotation and Formalin-
ether
Ancylostoma Duodenale o Increase positive
Slightly larger than N. findings significantly
americanus o Recommended
Single-paired male and - Culture methods
female reproductive organs
Head continues on the same Ex. Harada- Mori allow
direction as the body hatching of larvae from
curvature Left: Ancylostoma duodenale
eggs
Right: Necator americanus
(Filariform larva)
 Buccal capsule has 2 pairs of o Identification of
curved ventral teeth filariform larvae
o Studies: usually N.
americanus

3.Trichinella Spiralis Larva Actual Slide Clinical symptoms arise from successive phases of: Diagnosis is usually
Parasitic enteric invasion, made based on clinical
CN: Pork Worm Larval migration, and symptoms, and is
Disease: Trichinosis Muscle encystment confirmed by serology
MOT: Ingestion of o Asymptomatic: <10 larvae/g of muscle; or identification of
undercooked meat o May be life threatening: >50 larvae/g of muscle; encysted or non-
Infective Stage: Encysted Marked local and systemic hypersensitivity reaction to encysted larvae in
Larvae encysted larva with fever and hypereosinophilia biopsy or autopsy
Hosts: Different animal hosts: Periorbital and facial edema specimens.
Mostly mammals 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
4. Strongyloides Stercolaris Actual Slide: Three phases of infection: Clue: unexplained
Filariform Larva 1. Invasion of the skin by filariform larvae erythema, eosinophilia
pruritic, hemorrhagic papules Repeated
Free-living rhabditiform and 2. Migration of larvae through the body lobar pneumonia concentration
parasitic filariform stages with hemorrhages techniques:
Disease: Stronglyloidiasis, 3. Penetration of the intestinal mucosa by adult female Harada-Mori culture
Cochin-China Diarrhea worms (may occur together to cause hyperinfection) practical, low cost for
Permits AUTOINFECTION Light infection: no intestinal symptoms mass screening
Infective Stage: Filariform Moderate infection: diarrhea-constipation Baermann funnel
Larva Internet: Baeles string test
 MOT: Skin penetration, Heavy infection: intractable, painless, intermittent watery Duodenal aspiration
autoinfection (more fecally and bloody diarrhea (Cochin-China diarrhea) Small bowel biopsy
transmitted than soil- Some Complications: Disseminated
transmitted helminth) o edema infection: sputum,
Habitat: Small intestines o emaciation urine
(duodenum and upper o loss of appetite Serology but may cross
jejunum) but may be all o anemia react with filarial
throughout the alimentary o lobar pneumonia
tract. o malabsorption leading to cachexia

CESTODES
1. Diphyllobothrium latum Actual Slide (OVA) Actual Slide (Gravid Segment) Infections are usually limited History of residence or
ova and Gravid Segment to one worm travel to endemic areas,
Symptomatic due to absorbed raw fish diet
CN: Broad Fish Tapeworm toxins or by byproducts of
Disease: Diphyllobothriasis degenerating proglottids or Lab: Pernicious type of
Infective stage: Plerocercoid mucosal irritation anemia (to differentiate
larva or Sparganum Hyperchromic, megaloblastic it from Diphyllobotriasis
First Intermediate Host: anemia (defects in examination of gastric
Copepod maturation) with juice free HCl is useful)
Second Intermediate Host: thrombocytopenia and PA- achlorhydia
Fish (ex. Minnow, small leukopenia
freshwater fish) Anemia similar to pernicious Definitive diagnosis:
Definitive host: Man, dog, cat, anemia (bothriocephalus Fecalysis (kato
etc.(Plerocercoid attaches to anemia) technique)
the mucosal wall,matures in 3 Jejunum: competition with Characteristic:
weeks. the host for cobalamin operculated eggs,
Adult: (content is 50x that of T. proglottids, scolex
Spatulate scolex, 2 bothria saginata)
or sucking grooves With treatment, worms are
Long neck pushed down the intestines;
Mature proglottids 2-4 mm anemia is relieved
long, 10-12 mm wide with Internet:
Internet:
one set of reproductive
organs
Proglottids disintegrate only
when reproductive function
is completed
Eggs:
 Yellowish brown, moderately
thick shell, inconspicuous
operculum, small knob-like
opening
TREMATODES
1. Paragonimus Westermani Actual Slide Differentials: Pulmonary. TB, bronchiectasis, lung abscess, pleural Radiographs
Ova effusion -May aid in diagnosis but
difficult to differentiate
MOT: Eating raw or Chief Complaint: Cough, hemoptysis, difficulty of breathing paragonimiasis from PTB
insufficiently cooked and
infected Sundathelpusa crabs In the lungs, paragonimus worms provoke granulomatous reaction, Definitive Diagnosis
Common in Sorsogon gradually proceeding to development of fibrotic encapsulation. Detection of eggs in
(Southern Luzon area) Within the cyst, is blood-tinged purulent material containing eggs. sputum or stool; less
Pathogenesis is mostly in the Early stages are asymptomatic frequently in aspirated
lungs Internet Source: Dry cough, later producing blood stained or rust colored material from abscess or
Infective Stage: Metacercaria sputum with foul fish odor, most pronounced in the morning pleural effusion
Chest pains, dyspnea, hemoptysis Paragonimiasis
Egg: Oval, yellowish, brown, Low grade fever, fatigue, generalized myalgia Antigen Intradermal
thick shelled. Has flattened Chronic cough Skin test screening
but prominent operculum. Cerebral involvement-most serious complication, causing process, cannot
First Intermediate Host: Jacksonian epilepsy, cerebral hemorrhage, edema, visual differentiate past and
Antemelania asperata and disturbances, meningitis. present infections
Antemelania dactylus (snails) Clinical symptoms are less severe after five to six years, Serology diagnosis
Seccond Intermediate Host: although worms are known to persist longer of extrapulmonary
Mountain Crab Prognosis with light infections is good. Prognosis unfavorable in paragonimiasis
(Sudenthelphusa philippina) heavy infections and with cerebral involvement.

PROTOZOAN
1.Plasmodium falciparum Actual Slide: Pathological Process in the ERYTHROCYTE CYCLE Labs: leucocytosis,
gametocyte coagulopathy,
P falciparum merozoites reduce RBC deformability due to the thrombocytopenia,
Protozoan, Pigment rigidity of the parasite, changes in the RBC exoskeleton, increase prolonged ProTim/
Producing, Ameboid in membrane stiffness and cytoplasmic viscosity. RBC easily aPTT, decreased
Most common definitive ruptures fibrinogen
Host: Anopheles minimus RBC altered membrane transport soluble antigens of P.
flavirostri. Can also be hosted falciparum are potent inducers of pro/anti-inflammatory
by A. litralis, A. maculates, A. cytokines form monocytes and macrophages
mangyanus In P. falciparum, there is severe normocytic normochromic
Disease: Malaria anemia, bleeding, DIC, hemoglobinuria (black, brown, red)
 P. malariae has the longest erythrocytic cycle
Asexual Cycle: In P. falciparum, only ring form can be seen in microscope for
Occurs in man, the vertebrate diagnostic purpose. Occasionally, you will see gametocytes that
and intermediate Host are banana-shaped
Schizogony Merozoites
Gametogony Gametocytes CLINICAL:
MALARIA
Sexual Cycle: Considered the most important parasitic disease affecting man
Anopheles mosquito, the transmitted by the bite of infected Anopheles mosquito
invertebrate and definitive P. falciparum (70% of cases)
host P. vivax (<30%)
Sporogony sporozoites P. ovale
P. malariae (1%)
Higly endemic in Palawan, P.knowlesi (initially there is only animal-to-animal
Kalingaa, Apayao, Agusan del transmission, but now, it is known that it can be
sur, Ifugao. MDR malaria can transmitted to humans)
be found in Davao del Norte, It depends on the species when it comes to invasion. P.
Campostela Valley, Palawan falciparum can invade young and old RBCs, so only this species
can manifest severely. P. malariae prefers old RBCs
Internet Source:

2. Entamoeba Histolytica Internet Sources: The clinical spectrum ranges from asymptomatic infection, It can be diagnosed
(No actual slide for this) diarrhoea and dysentery to fulminant colitis and peritonitis as by stool samples, but
well as extraintestinal amoebiasis. it is important to
Infective Stage: Non invasisve note that certain
infection: Cysts, Invasive Acute amoebiasis can present as diarrhoea or dysentery with other species are
Infection: Trophozoites frequent, small and often bloody stools. Chronic amoebiasis can impossible to
Transmission: Transmission present with gastrointestinal symptoms plus fatigue, weight loss distinguish by
occurs via the faecaloral and occasional fever. Extraintestinal amoebiasis can occur if the microscopy alone.
route,. parasite spreads to other organs, most commonly the liver where Trophozoites may be
Pseudopod-forming it causes amoebic liver abscess. Amoebic liver abscess presents seen in a fresh fecal
nonflagellated protozoan with fever and right upper quadrant abdominal pain. smear and cysts in
parasite, for movement an ordinary stool
Most invasive of the sample. ELISA or RIA
entamoebidae family 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 Usually not found in the peripheral
multiple infection of RBC is commom. circulation, but they are showm in
They often show double chromatin the final stage of severe infection.The
dots and parasitized red cells are not mature schizont form 18 to 24 Macrogametocyte of P. Falciparum
enlarged and may contain Maurers merozoites.
Ring Forms of Plasmodium falcifarum
dot( but not seen here).
 P. Falciparum.The female The male gametocyte is less pointed
gametocyte is cresentic or banana and stains more lightly than the
shaped and is called crescent. female gametocyte P. Falciparum. Thick blood Smear Micogametocyte of P. Falciparum
Cytoplasm is stained blue and with Giemsa Stain
nucleus red by Giemsa Stain.

Liver of an autopsy case of falcifarum

malaria infection. 37 year old man,
infected and onset began in Africa; Spleen of an autopsy case of
then he was sent back to Japan. Section of the liver.Degenaetaion of falcifarum malaria infection. Marked
Diagnosis was not established until hepatic cells and malarial pigment in Section of the spleen. The presence of
splenomegaly is seen and parasite
shortly before death.Liver is Kupffers cells are seen. malarial pigment is present.
density in peripheral blood shortly
enlarged. before death was 9x105 /mm3