Chapter 11 INTRODUCTION TO PARASITOLOGY

5.

ERRATIC PARASITES: become fixed in an unusual organ different from that which is ordinarily parasitized (e.g. ASCARIS LUMBRICOIDES) Essential to the existence of parasites Harbors the parasite and provides nourishment to the parasite

HOSTS SYMBIOSIS a form of relationship in which UNLIKE organisms exists TOGETHER. TYPES OF SYMBIOSIS: COMMENSALISM - TWO SPECIES live together and ONE SPECIES BENEFITS from the other WITHOUT HARMING OR BENEFITING THE OTHER. MUTUALISM - TWO organisms MUTUALLY BENEFITS each other. PARASITISM ONE BENEFITS to the DETRIMENT OF THE OTHER.

TYPES OF HOSTS IN A PARASITIC RELATIONSHIP: (DRIP)

1.

2.

3.

PARASITES BASED ON: HABITAT:

1. 2. ECTOPARASITES: live OUTSIDE of the hosts body. (e.g fleas, lice) ENDOPARASITES: live INSIDE of the body of the host e.g. helminths or worms) 4.

DEFINITIVE HOSTS: adult stage of the parasite SEXUAL STAGE or the sexual phase of the life cycle of the parasite occurs. INTERMEDIATE HOSTS: harbor the larval ASEXUAL STAGE of the parasites life cycle occurs. RESERVOIR HOSTS: VERTEBRATE HOSTS which harbor the parasite act as a SOURCE OF INFECTION IN MAN (e.g. pig for Balantidium Coli) PARATENIC HOSTS MEANS OF TRANSPORT (e.g. VECTORS) so that the infective state of a certain parasite may reach its final host.

INFESTATION: INVASION of the body by ECTOPARASITES , in which the parasite establishes itself upon the host. INFECTION: INVASION of the body by ENDOPARASITES and is the result of entry and multiplication of the parasite within the host.

SOURCES OF EXPOSURE TO INFECTION OR INFESTATION:

1. 2. 3. 4. 5. 6. Contaminated soil or water Food containing the infective state of the parasite Blood-sucking insect Animal harboring the parasite Another person, his clothing, bedding or the immediate environment that he has contaminate Self

ABILITY TO LIVE INDEPENDENTLY:

1. 2. FACULTATIVE PARASITES: can live independently of the host (free living) Dont have to live as parasites inside a host. OBLIGATE PARASITES: must exist as parasites inside a host (e.g PLASMODIUM, LEISHMANIA, HOOKWORMS)

MODE OF LIVING: ( IT PIE)

1. 2. 3. 4. PERMANENT PARASITES: remain in a host from early life to maturity (e.g. PLASMODIUM) INTERMITTENT PARASITES: visit the host during feeding time (e.g. NON-PATHOGENIC PARASITES) INCIDENTAL PARASITES: occur on an unusual host (e.g. DOG TAPEWORM IN HUMANS) TRANSITORY PARASITES: larva developes in a host while the adult free-living (e.g. ECHINOCOCCUS GRANULOSUS or the DOG TAPEWORM)

SOURCES OF EXPOSURE TO INFECTION OR INFESTATION:

SOIL with human excreta Most common source of infection Ascaris lumbricoides Trichuris trichiura Human hookworms Stronglyoides Stercoralis Viable cyst of: Parasitic amebae Intestinal flagellates Taenia Solium eggs Infective state of: human blood flukes Diphyllobothrium latum as well as other intestinal & liver flukes Trichinella spiralis Taenia solium Taenia Saginata

MODES OF TRANSMISSION
INGESTION of contaminated food & water DRINKING OF CONTAMINATED WATER (all in the embryonated egg stage) Most common mode of transmission Intestinal protozoa (cyst) Dwarf tapeworm HYMENOLEPIS NANA Round worms: ASCARIS LUMBRICOIDES TRICHURIS TRICHIURA ENTEROBIUS VERMICULARIS TRICHINELLA SPIRALIS TAENIA SOLIUM, TAENIA SAGINATA, DIPHYLLOBOTHRIUM LATUM INTESTINAL FLUKES LUNG FLUKE OTHER ROUNDWORMS- such as hookworms & Strongyloides malaria, leshmaniais, Trypanosomiasis filariasis ENTEROBIUS VERMICULARIS or the pinworm TOXOPLASMA GONDII and occasionally with malarial parasites STRONGYLOIDES ANCYLOSTOMA TRICHOMONAS VAGINALIS

WATER

FRESH WATER FISH

Source for the fish tapeworm

EATING FOOD containing the mature larval stages

RAW PORK IMPROPERLY COOKED OR RAW BEEF BLOOD SUCKING INSECTS Female ANOPHELES mosquito SANDFLY TSETSE FYL REDUVIID BUG CULEX MOSQUITO DOGS

malaria leishmaniasis trypanosomes trypanosomes Filariae

ENTER THROUGH THE BODY from the soil via the SKIN from fresh water BITE OF BLOODSUCKING ARTHOPODS such as mosquitos INHALATION OF AIRBORNE EGGS TRANSPLACENTAL OR CONGENITAL INFECTION TRANSMAMMARY (MILK) INFECTION with species of SEXUAL INTERCOURSE

Direct source of Echinococcus infection with the granulosus hydatid cyst of Other Pathogenic ameba ENTAMOEBA human HISTOLYCA beings Pinworm ENTEROBIUS VERMICULARIS Dwarf tapeworm- HYMENOLEPIS NANA AUTOINFECTION accounts for some of the infections and some reinfection with STRONGYLOIDES STERCORALIS

PORTAL OF EXIT OF PARASITES ANUS- most common portal of exit of parasites URINE Eggs of roundworms are excreted with human feces and contaminate soil & water TRICHOMONAS VAGINALIS STRONGLYOIDES STERCORALIS SCHISTOSOMA HAEMATOBIUM PARAGONIMUS WESTERMANI (lung fluke) Common round worm ASCARIS LUMBRICOIDES (larval stage) TRICHOMONAS VAGINALIS LYTIC NECROSIS ENZYMES produced by many parasites that are necessary for them to digest food available in the immediate environment may CAUSE HARM TO THE HOST TISSUES. An example is that of ENTAMOEBA HISTOLYTICA, which LYSES tissues for nutritional needs and penetrates into the tissues of the colon and extraintestinal viscera. STIMULATION OF HOST TISSUE REACTION: HOOKWORM INFECTION or MALARIA destruction of RBC Blood Fluke SCHISTOSOMA JAPONICUM may lead to development of CANCER OF THE LIVER Fluke CLONORCHIS SINENSIS may cause BILIARY DUCTS CANCER TOXIC & ALLERGIC PHENOMENA: Proteins or other metabolites produced by the parasites may lead to hypersensitivity reactions due to stimulation of antibody productions Pinworm infection ENTEROBIUS VERMICULARIS manifests PRURITUS ANI CLASSIFICATIONS OF PARASITES: PROTOZOA METAZOA (helminths) Single-celled multicellular Four Major Groups Based on Two PHYLA: MOTILITY 1. PLATYHELMINT 1. SARCODINA HES (flatworms) (amebas) 2. NEMATHELMINT 2. SPOROZOA HES (sporozoans) (roundworms or 3. MASTIGOPHORA nematodes) (flagellates) 4. CILIATA (ciliates) Phylum PLATYHELMINTHES is further divided into 2: 1. CESTODA (tapeworms) 2. TREMATODA (flukes)

SPUTUM

SEXUAL INTERCOURSE

PATHOGENESIS OF PARASITIC INFECTIONS: PATHOGENESIS The dynamics of any disease process. 1. 2. 3. 4. 5. Trauma or physical damage Lytic necrosis Stimulation of host tissue reaction Toxic & allergic phenomena Opening of pathways for entry of other pathogens into the tissues

INAPPARENT INFECTION No symptoms & no detectable harm Can remain inapparent continuosly for long periods or between short periods of relapse (e.g. malaria) For most helminthic (worms) infections, s/sx usually manifest only if large numbers of the worms are present. TRAUMATIC DAMAGE Entry of the INFECTIVE LARVAE OF HOOKWORMS or BLOOK FLUKES into the skin may produce relatively SLIGHT PHYSICAL DMG SMALL LESSIONS may result from the BITE OF MOSQUITOES (as in malaria) and other insects, such as the TSETSE FLY which causes AFRICAN SLEEPING SICKNESS. LARVAL STAGE of certain roundworms (ASCARIS OR HOOKWORMS) may lead to RUPTURE OF THE PULMONARY CAPILLARIES. Large worms such as ASCARIS LUMBRICOIDES OR TAENIA SAGINATA may produce ACUTE INTESTINAL OBSTRUCTION.

CHAPTER 11 SELF-ASSESSMENT QUESTIONS

1. A type of symbiotic relationship in which two organisms benefit from each other: 2. A parasite transmitted through the mothers milk: 3. A type of host where the adult stage of the parasite develops: 4. Infection with these parasite can lead to the development of cancer: 5. Autoinfection can be seen in infection of this parasite: 6. Urine may serve as the portal of exit for these parasites: 7. The most common source of parasitic infection is: 8. The most common portal of exit of parasite is: 9. Parasite that can live independently of the host are described as: 10. Parasites produce disease by the following mechanisms:

Chapter 12 PROTOZOA
PROTOZOA Single-cell Spherical to oval or elongated Belong in KINGDOM PROTISTA 4 MAJOR SUBDIVISIONS OR PHYLA: 1. SARCODINA o AMOEBAS move by means of PSEUDOPODIA (false feet) 2. APICOMPLEXA class SPOROZOA o PROTOZOA have NO MEANS of locomotion, and therefore DO NOT MOVE 3. MASTIGOPHORA o Move by means of SPECIAL HAIR-LIKE PROJECTIONS of the cytoplasm called FLAGELLA 4. CILIOPHORA o Move by means of CILIA, small thread-like structures distributed over the surface of the body of the parasite

MODE OF TRANSMISSION: Intestinal & Luminal Protozoa

Person-to-person Ingestion of contaminated food & water Blood & Tissue Protozoa Direct contact Vectors (i.e. Anopheles mosquito for malaria CYST = The DORMAT/ NON-MOTILE STAGE BUT INFECTIVE STAGE or the stage of the parasite that enters the host TROPHOZOITE = The ACTIVE or PATHOGENIC STAGE/ DIVIDING STAGE or the stage that is responsible for DISEASE PRODUCTION

FACULTATIVE PARASITES capable of a free-living state. Normally reside in the soil or water, but can cause serious illness when they gain entrance to the CNS or to the eyes Examples: ACANTHAMOEBA SPP. NAEGLERIA FOWLERI

REPRODUCTION: Repeated asexual multiplication through BINARY FISSION o SARCODINA o MASTIGOPHORA Union of two cells, a process called SYNGAMY

PHYLUM SARCODINA 1. Entamoeba Histolyca

DISEASE Amebiasis 1. Acute intestinal amebiasis presents as dysentery (bloody, mucus-containing diarrhes) accompanied by lower abdominal discomfort, flatulence, and tenesmus. Chronic infection may occur w/ symptoms such as occasional diarrhea, wt. loss, & fatigue. In some patients, a granulomatous lesion called AMEBOMA may form in the cecum or in the rectosigmoid area of the colon. This can resemble a malignant tumor of the colon 2. Amebic abscess of the liver is characterized by RUQ pain, wt loss, fever & a tender enlarged liver. The abscess has a characteris ANCHOVY-SAUCE appearance. Abscesses found on the rt lobe of the liver may penetrated the diaphragm & cause LUNG CANCER

IMPORTANT PROPERTIES Intestinal protozoan Life cycle consists of two stages cyst (non-motile) & trophozoite (motile)

PATHOGENESIS & EPIDEMIOLOGY Acquired by INGESTION OF ITS CYSTS (INFECTIVE STAGE) in contaminated food & water primarily FECAL-ORAL ROUTED Trophozoites secrete enzymes that cause local necrosis producing FLASK-SHAPED ulcer Development of abscess in the LIVER More common in tropical countries esp. poor sanitation areas

LABORATORY DIAGNOSIS Diarrheal stools should be examined within one hour of collection to see the motility of the throphozoite Serologic testing may be useful for the dx of invasive amebiasis

TREATMENT DOC for symptomatic intestinal amebiasis or hepatic abscess is METRONIDAZOLE or TINIDAZOLE for 10 days Asymptomatic cyst carriers should be treated with IODOQUINOL or PAROMOMYCIN

PREVENTION Avoiding fecal contamination of food & water Good personal hygiene such as proper handwashing Purification of water source Adequate cooking of vegetables Avoiding the use of night soil (human feces) for fertilization of crops.

2.

Acanthamoeba Castellani & Naegleria Fowleri

Minor protozoan pathogens Free-living Causes meningoencephalitis

Found in soil & freshwater lakes ACANTHAMOEBA survive in COLD WATER carried into the skin or eyes during trauma. It causes MENINGOENCEPHALITIS & KERATITIS, an inflammation of the cornea, primarily 8in patients who wear contact lenseInfection primarily occurs in IMMUNOCOMPROMISED INDIVIDUALS NAEGLERIA survive in THERMAL SPRING WATER acquitted intranasally when swimming in contaminated water. It penetrates the nasal mucosa & cribriform plate to produce rapidly FATAL MENINGITIS & ENCEPHALITIS. Infection occurs in HEALTHY INDIVIDUALS, USUALLY CHILDREN INFECTIVE STAGE: Cyst PATHOGENIC STAGE: Trophozoite

Finding the organism in CSF

NAEGLERIA Infections: AMPHOTERICIN B ACANTHAMOEBA Infections: PENTAMIDINE, KETOCONAZOLE, or FLUCYTOSINE. Prognosis is poor even with treatment

For ACANTHAMOEB Infection: Adequate boiling of water. Wearing of mask while cleaning (dust also carries the cyst) Regular disinfection of contact lenses No known means of prevention & control for NAEGLERIA Infection

PHYLUM SARCOMASTIGOPHORA 1. Giardia Lamblia

DISEASE Giardiasis Non-bloody, foul-smelling diarrhea accompanied by nausea, anorexia, flatulence, & abdominal cramps persisting for weeks or months. Malabsorption of fat may lead to the presence of fat in the stool (STEATORRHEA) of the patient. Patient is AFEBRILE

IMPORTANT PROPERTIES Life Cycle: TROPHOZOITE: pearshaped with 4 pairs of flagella CYST: oval & thick-walled with 4 nuclei. Each cyst gives rise to 2 trophozoites during excystation in the intestinal tract

2.

Trichomonas Vaginalis

Trichomoniasis Infection in women leads to VAGINITIS with a watery, foul-smelling, greenish vaginal discharge accompanied by itching (PRURITUS) & burning sensation. Cervix is very red, with small, punctuate haemorrhages giving rise to a STRAWBERRY CERVIX. Infection in men is usually asymptomatic. Some may manifest with symptoms of URETHRITIS or PROSTATITIS

Pear-shaped organim with a central nucleus & 4 anterior flagella. Exists only in the TROPHOZOITE form (INFECTIVE & PATHOGENIC FORM)

PATHOGENESIS & EPIDEMIOLOGY Ingestion of the cyst in focally-contaminated water & food. Trophozoite attaches to the wall of the gut but does not invade. Instead, inflammation of the duodenal mucosa occurs, leading to malabsorption of protein & fat. Asymptomatic & occur in outbreaks related to contaminated water supplies. Mammals & humans act as the reservoirs Common in male homosexuals as a result of oral-anal contact. High incident in daycare centers & patients in mental hospitals. Transmitted mainly by SEXUAL CONTACT. Primarily located in the VAGINA & PROSTATE Infection is one of the most common worldwide Frequency is highest among SEXUALLY-ACTIVE WOMEN in their 30s and lowest in POSTMENOPAUSAL WOMEN

LABORATORY DIAGNOSIS Finding trophozoites, cysts, or both in diarrheal stools. Asymptomatic carriers stools may show cysts only If microscopic exam is negative, string test may be done, which consists of swallowing a weighted string until it reaches the duodenum. Trophozoites adhere to the string & can be visualized after withdrawal of the string.

TREATMENT DOC is METRONIDAZOLE or QUINACRINE HYDROCHLORIDE

PREVENTION Drinking boiled, filtered, or iodine-treated water in endemic areas. Proper hygiene & waste disposal must also be observed. No prophylactic drug or vaccine is available.

Visualization of TROPHOZOITE in a wet mount of vaginal or prostatic secretions

DOC is METRONIDAZOLE

To prevent ping pong infections, there should be simultaneous tx of both sexual partners. Maintenance of the low pH of the vagina is also helpful. Use of condoms can limit transmission of the parasite. Health & sex education are also important

3.

Leishmania Donovani

Kala-azar (Visceral Leishmaniasis) ~~Visceral involves the body organs Kala-azar means BLACK SICKNESS Begins with intermittent fecer, weakness, & wt loss. Massive enlargement of the spleen (SPLENOMEGALY) is characteristic leading to HYPERSLENISM and resulting in ANEMIA In light-skinned patients, hyperpigmentation of the skin may be seen Involvementof the BONE MARROW results in further ANEMIA LEUCOPENIA & THROMBOCYTOPENIA, predisposing the patient to INFECTION & GASTROINTESTINAL BLEEDING. Untreated disease is almost always FATAL due to secondary infection.

Vector: FEMALE SANDFLY (PHLEBOTOMUS SPECIES) Sandfly sucks blood from an infected host, ingesting macrophages containing AMASTIGOTES AMASTIGOTES differentiates into PROMASTIGOTES (INFECTIVE STATE) in the GUT of the SANDFLY and are then transmitted to an uninfected human during the next bite PROMASTIGOTES are engulfed by MACROPHAGES, in which they transform into AMASTIGOTES (PATHOGENIC STAGE) Infected cells die & release amastigotes that infect other macrophages & reticuloendothelial cells

Mode of transmission: BITE OF THE VECTOR Organs of the reticuloendothelial system (LIVER, SPLEEN, & BONE MARROW) are the most severely affected Found in several areas of the world,including the Mediterranean basin, Middle East, China & some parts of Africa

Finding AMASTIGOTES in a BONE MARROW, SPLEEN, or LYMPH NODE BIOPSY preparation SEROLOGIC TESTING can be done (very high concentration of IgG is indicative of infection) Skin test is available using a CRUDE HOMOGENATE of PROMASTIGOTES (LESHMANIN) as the antigen

DOC is SODIUM STIBOGLUCONATE Mortality rate is reduced to 5% with proper therapy Infection confers PERMANENT IMMUNITY after recovery

Prevention of the bite from the SANDFLY Wearing of protective clothing, use of netting, & use of insect repellants. Insecticide spraying may also be done to kill the sandfly

4.

Leishmania Tropica & Leshmania Braziliensis

5.

Trypanosoma Cruzi

Cutaneous Leishmaniasis & Mucocutaneous Leshmaniasis CUTANEOUS LESHMANIASIS: starts as a red papule at the bite site, usually on an exposed extremity. This enlarges to form multiple satellite nodules that coalesce and ulcerate MUCOCUTANEOUS LESHMANIASIS begins with a papule at the side of the bite, then forms metastatic lesions, usually at the mucocutaneous junction of the nose & mouth. Disfiguring granulomatous, ulcerating lesions destroy the nasal cartilage (TAPIR NOSE) but not the adjacent bone. DEATH can occur from secondary infection Chagas Disease (American Trypaosomiasis) Acute phase = FACIAL EDEMA (ROMANIAS SIGN & A NODULE (CHAGOMA) near the bite site Accompanied by fever, LYMPHAFRNOPATHY, and HEPATOSPLENOMEGALY CARDIAC MUSCLE is severely affected tissue & the disease often results in MYOCARDITIS and CARDIAC ARRYTHYMIAS Loss of tone of the colon (MEGACOLON) and the esophagus (MEGAESOPHAGUS) DEATH is due to cardiac arrhythmias & failure

Vector: SANDFLY Mode of Transmission: Bite from SANDFLY Reservoir: FOREST RODENTS Life cycle are the same as of the L. Donovani

Vector: REDUVIID BUG (TRIATOMA, CONE NOSE or KISSING BUG) Reservoir Hosts: Humans & Animals) Infective State: TRYPOMASTIGOTE & the Pathogenic Stage: AMASTIGOTE Mode of Transmission: Defacation of the Kissing bug in the corner of a persons eye Blood transfusion Organ implantation Bite of the vector

L. TROPICA causes cutaneous leishmaniasis (ORIENTAL SORE, DELHI BOIL). Endemic in Middle East, Africa, ad India L. BRAZILIENSE causes mucocutaneous leishmaniasis (ESPUNDIA). Occurs mostly in Brazil and Central America; primarily in construction & forestry workers Lesions are confined to the skin in cutaneous leishmaniasis and to the mucous membranes, cartilage & skin in mucocutaneous leishmaniasis NECROTIC ULCER forms at the site of the bite which tends to become secondarily infected with bacteria Diff cell types may be affected but glial, reticuloendothelial & esp myocardial cells are the most frequently affected Primarily occurs in rural Central & So America Acute disease occurs rarely in USA but the chronic form is seen with increasing frequency in immigrants from Latin America Primarily seen in rural areas because the REDUVIID BUG LIVES IN THE WALLS OF RURAL HUTS & FEEDS AT NIGHT.

Presence of AMASTIGOTES in a SMEAR taken from the SKIN LESION LEISHMANIN SKIN TEST is positive when the skin ulcer appears

DOC is SODIUM STIBOGLUCONATE but results are usually unsatisfactory

Protection from sandfly by using netting, window screens, protective clothing and insect repellent

Trypomastigote in thick or thin films of the patients blood Other Dx methods: bone marrow aspiration or muscle biopsy, culture on special medium, xenodiagnosis which consists of allowing an uninfected lab-raised reduviid bug to feed on the patient, and after several weeks, examining the intestinal contents of the bug for the organism Serologic tests can also be helpful Xenodiagnosis & Serologic tests are useful in the dx of the chronic form

DOC for the acute phase is NIFURTIMOX. Alternative drug is BENZNIDAZOLE. There is no effective drug against the chronic form

Protection from the bite of the reduviid bug Improvement of housing conditions Insect control

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6.

T. Brucei Gambiense & T. Brucei Rhodesiense

PHYLUM APICOMPLEXA 1. Toxoplasma Gondii

African Sleeping Sickness Initial lesion is an indurated skin ulcer (TRYPANOSOMAL CHANCRE) at the bite site Intermittent weekly fever & lymphadenopathy then develop Enlargement of the posterior lymph nodes (WINTERBOTTOMs SIGN) is commonly seen. ENCEPHALITIS is characterized by headache, insomnia, & mood changes. Muscle tremors, slurred speech, and apathy follow, progressing to somnolence (sleeping sickness) and coma Untreated disease is fatal as a result of pneumonia DISEASE Toxoplasmosis Some resemble infectious mononucleosis with fever, jaundice & intracranial calcifications Congenital infection results in abortion, stillbirth, or neonatal disease w/ encephalitis, chorioretinitis, and hepatosplenomegaly Causes BLINDNESS in CHILDREN Infection in immunocompromised patients lead to LIFETHREATENING disseminated disease

Both species are similar in morphology & life cycle Life cycle involve the TSETSE FLY (GLOSSINA) as the vector Humans are the reservoir for T. GAMBIENSE, while domestic animals esp cattle & wild animals serve as the reservoirs for T. RHODESIENSE Infective & pathogenic stage is the TRYPOMASTIGOTE

TRYPOMASTIGOTES spreas from the skin through the blood to the lymph nodes & the brain. Demyelinating encephalitis occurs leading to the characteristic manifestations of the disease Endemic in sub-saharan Africa, the natural habitat of the TSETSE FLY, T. GAMBIENSE causes disease along water courses in west Africa, wheres T RHODESIENSE is found in the arid regions of East Africa

Microscopic exam of the blood reveals TRYPOMASTIGOTES during the early stages of the disease Aspiration of the chancre or enlarged lymph nodes may also reveal parasites Involvement of the CNS will lead to demonstration of the parasite in the CSF Serologic tests can also be helpful

Most effective drug s SURAMIN. However, tx must be initiated before encephalitis develops because the drug cannot penetrate the blood-brain barrier well. PENTAMIDINE is an alternative drug, especially if CNS symptoms are present Tx with PENTAMIDINE followed by MELARSOPROL is recommended

Protection against the bite of the TSETSE FLY Use of netting & protective clothing are recommended. Clearing the forest around the villages and using insect repellants are also helpful measures. No vaccine is available

IMPORTANT PROPERTIES Definitive Host: Domestic Cat & other felines Intermediate Hosts: humans & other mammals Mode of Transmission: Ingestion of cysts (OOCYSTS) in UNDERCOOKED MEAT OR FROM CONTACT WITH CAT FECES In the small intestine, these cysts rupture into trophozoites (tachyzoites or bradyzoites) Parasite enters host cells in the brain, muscle & other tissues where they develop into cysts

PATHOGENESIS & EPIDEMIOLOGY Human Infection: eating undercooked meat (e.g lamb& pork) from animals that grazed in soil contaminated w/ infected cat feces TRANSPLACENTAL TRANSMISSION from an infected mother to the fetus CONGENITAL infection of the fetus occurs only the mother is infected during pregnancy Infxn occurs worldwide, usually sporadic, but outbreaks associated w/ ingestion of raw meat or contaminated water

LABORATORY DIAGNOSIS Acute & Congenital infection involves IMMUNOFLOURESCENCE assay for IgM antibodies Microscopic examination of GIEMSA-STAINE preparations shows CRESCENT-SHAPED TROPHOZOITES during the acute infection Cysts may be seen in the tissue

TREATMENT Congenital toxoplasmosis is treated with a COMBINATION of SULFADIAZINE and PYRIMETHAMINE This is also the tx regimen for disseminated disease in immunocompromised patients Acute toxoplasmosis in immuncompromised individuals is usually SELFLIMITED but patiens with CHORIORETINITIS should be treated

PREVENTION Thorough cooking of meat to kill the cysts Pregnant women should refrain from eating undercooked meat & should avoid contact with cats & refrain from handling litter boxes. Cat should not be fed raw meat

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2.

Plasmodium spp

Malaria 3 STAGES: cold stage, hot stage, & the sweating stage ABRUPT ONSET OF CHILLS accompanied by headache, myalgias, and arthralgias. SPIKING FEVER follows, reaching up to 41C, accompanied by shaking chills, nausea, vomiting, and abdominal pain This is then followed by DRENCHING SWEATS Patients usually feel well btwn febrile episodes. SPLENOMEGALY is often present and ANEMIA is prominent Infxn with P. FALCIPARUM is potentially LIFETHREATENING as a result of extensive BRAIN (CEREBRAL MALARIA) and KIDNEY DAMAGE The DARK COLOR OF URINE gave rise to the term BLACKWATER FEVER Malaria caused by other three plasmodia is usually self-limited, with low mortality rate. RELAPSES OF P. VIVAX & P. OVALE malaria can occur up to several years after the initial illness as a result of the latent hypnozoites in the lever.

Caused by 4 plasmodia: Plasmodium Vivax, Plasmodium Malariae, Plasmodium Ovale, & Plasmodium Falciparum. Vector & Definitive Host: FEMALE ANOPHELES MOSQUITO Intermediate Host: HUMAN Sexual Cycle (SPOROGONY) occurs primarily in mosquitos Asexual Cycle (SCHIZOGONY) occurs in humans Infective Stage: SPOROZOITE from the salia of the biting mosquito,which is taken up by the hepatocytes This exoerythrocytic phase leads to MULTIPLICATION & DIFFENTIATION of sporozoites into MEROZOITES P. VIVAX & P. OVALE produce a latent form called HYPNOZOITE in the liver, which is the CAUSE OF RELAPSES seen in VIVAX & OVALE MALARIA MEROZOITES are released from liver cells & infect red blood cells (ERYTHROCYTIC PHASE) which is eventually released to infect other erythrocytes. Periodic release of merozoites causes typical recurrent symptoms seen in malaria patients. Some merozoites then develop into male & femal

Main mode of transmission: BITE OF THE FEMALE ANOPHELES MOSQUITO from DUSK to DAWN Other mode of transmission: Placental transmission Blood transfusions Intravenous drug abuse Pathologic findings: Destruction of RBC P.PALCIFARUM infects both young & old RBC = causes the most SEVERE infection P. VIVAX & P. OVALE infects young RB P. MALARIAE infects primarily old RBC Timing of Fever Cycle: P.MALARIAE= 72 hrs, symptoms recur th every 4 day (QUARTAN MALARIA) Every third day (TERTIAN MALARIA) is subdivided into MALIGNANT TERTIAN MALARIA (P. Palcifarum) BENIGN TERTIAN MALARIA (P. Vivax & P. Ovale) Occurs worldwide, primarily in tropical & subtropical areas esp in Asia, Africa & Central & So America. Endemic in 75 out of 79 provinces in the Phils. Catanduanes,

Exam of GIEMSA STAINED SMEARS of the blood TROPHOZOITES are seen w/in the infected RBC P.PALCIFARUM show a CRESCENT-SHAPED or BANANA-SHAPED gametocytes If more than 5% of RBC are parasitized, the dx is usually P. FALCIPARUM MALARIA

DOC for acute malaria caused by sensitive strains is CHLOROQUINE. P.VIVAX & P.OVALE Chloroquine resistant = PRIMAQUINE P.FALCIPARUM Chloroquine resistant= MEFLOQUINE or combination of QUININE & DOXYCYCLINE In severe cases (CEREBRAL MALARIA or BLACKWATER FEVER), PARENTERAL QUINIDINE or QUININE is used

CHEMOPROPHYLAXIS of malaria for travellers to endemic areas consists of MEFLOQUINE or DOXYCYLINE. Travelers to areas where the other plasmodia are found should take CHLOROQUINE starting 2 WKS before arrive & continued for 6wks after departure, followed by a 2wk course of PRIMAQUINE if exposure was high Other preventive measures inc avoidance of the bite of vector through the use of mosquito netting, window screens,protective clothing, & insect repellants Insecticide sprays, as well as DRAINAGE OF STAGNANT WATER inm swamps, and ditches. NO VACCINE available

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gametocytes. The gametocyte-containing RBCs are then ingested by the vector where sexual reproduction of the parasite takes place

Cebu, Bohol & Leyte are malaria-free. High endemicity in Palawan, KalingaApayao, Ifugao & Agusan del Sur

PHYLUM CILIOPHORA 1. Balantidium Coli

DISEASE

IMPORTANT PROPERTIES Largest protozoan to infect humans Found worldwide Main Reservoir Hosts: Domestic animals esp pigs Human infections occur through ingestion of the cysts (INFECTIVE STAGE) in food or Water contaminated with animal or human feces Trophozoites (PATHOGENIC STAGE) excyst in the small intestines & travel to the colon, producing an ulcer similar to that of ENTAMOEBA HISTOLYTICA Extraintestinal lesions do NOT occur

70% of cases are due to P.Falciparum PATHOGENESIS & EPIDEMIOLOGY Most infected individuals are asymptomatic Dysenteric type of diarrhea may occur

LABORATORY DIAGNOSIS Stool exam finding of large trophozoites or cysts with a characteristic of VSHAPED NUCLEUS in the stool

TREATMENT DOC is TETRACYCLINE Children less than 7yo is METRONIDAZOLE

PREVENTION Avoiding contamination of food & water by feces of domestic animals

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