Introduction of parasitology extraaa copy 1

PARASITOLOGY EXAM REVIEW 2015 BHAGATH M S RAJEEV BISWAS

Parasitology Exam Review 2015

CONTENTS Introduction of parasitology Chapter 45 LOBOSEA  Section 1 entamoeba histolytica Chapter 46 ZOOMASTIGOPHOREA  Section 1 trichomonas vaginalis  Section 2 giardia lamblia  Section 3 leishmania Chapter 47 SPOROZOA  Section 1 plasmodia  Section 2 toxoplasma gondii  Section 3 cryptosporidium Chapter 49 TREMATODES  Section 1 introduction  Section 2 clonorchis sinensis  Section 3 paragonimus spp  Section 4 schistosoma  Section 5 Fasciolopsis Buski, Chapter 50 CESTODES  Section 1 Introduction of cestodes  Section 2 Taenia solium,  Section 3 Taenia saginata  Section 4 Echinococcus granulosus  Section 5 spirometra mansoni Chapter 51 NEMATODA  Section 1 Introduction of Nematoda  Section 2 Ascaris  Section 3 trichiura,  Section 4 Hookworms  Section 5 Enterobius  Section 6 Filariae Chapter 52 ARTHROPODA  (Introduction of Arthropoda) Chapter 53 INSECTA  (Introduction)  Section 2 Mosquitoes,  Section 3 flies Chapter 54  Sarcoptes, Demodex

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Introduction of parasitology TERMS 1. SYMBIOSIS :: ALL LIVING ANIMALS ARE USED AS HABITATS BY OTHER ORGANISMS. BASED ON THE RELATIVE DEGREES OF BENEFIT OBTAINED BY EACH PARTNER FROM THE ASSOCIATION

2. COMMENSALISM :: IS THE ASSOCIATION OF TWO DIFFERENT ORGANISMS, IN WHICH ONE PARTNER IS BENEFITED WHILE THE OTHER IS NEITHER BENEFITED NOR INJURED, SUCH AS ENTAMOEBA COLI AND HUMAN. 3. MUTUALISM :: IS CHARACTERIZED BY RECIPROCAL BENEFIT BETWEEN THE TWO ORGANISMS INVOLVED. 4. PARASITISM :: IS THE ASSOCIATION OF TWO DIFFERENT ORGANISMS, IN WHICH ONE PARTNER IS BENEFITED WHILE THE OTHER IS INJURED, SUCH AS ASCARIS LUMBRICOIDES AND HUMAN. TWO PARTNERS OF PARASITE PARASITISM HOST 5. PARASITE :: IN PARASITISM, IT IS THE BENEFITED PARTNER. IT IS AN ANIMAL ORGANISM WHICH LIVES IN OR ON THE HOST IN ORDER TO OBTAIN NOURISHMENT AND SHELTER FROM THE HOST AS WELL AS DOES HARMS TO THE HOST. ENDOPARASITE

LIVES IN THE HOST

ASCARIS LUMBRICOIDES

ECTOPARASITE

LIVES ON THE SURFACE OF THE HOST

MOSQUITO, LOUSE

PERMANENT

WHICH MUST LIVE IN OR ON THE HOST

ASCARIS LUMBRICOIDES

---------------------------------

MOSQUITO

PARASITE TEMPORARY

(INTERMITTENT) PARASITE

OBLIGATORY PARASITE

A PARASITE WHICH CANNOT SURVIVE IN ANY OTHER MANNER

FACULTATIVE PARASITE

IS AN ORGANISM WHICH MAY EXIST IN A FREE-LIVING STATE OR AS A COMMENSAL AND WHICH MAY BECOME PARASITIC IF OPPORTUNITY PRESENTS

OPPORTUNISTIC PARASITE

THE PARASITE IN AN IMMUNOCOMPETENT HOST IS LOW VIRULENCE THAT SELDOM PRODUCES DISEASE, AND CAN’T BE DETECTED BY NORMAL EXAMINATION. BUT INFECTION IN AN IMMUNOCOMPROMISED

(SUCH AS AIDS…) HOST MAY BE MANIFESTED BY SEVERE DISEASE, SOMETIMES BE LETHAL. 6. HOST:: IN PARASITISM,IT SUPPLIES THE PARASITE WITH NOURISHMENT AND SHELTER, IT IS THE INJURED PARTNER. DEFINITIVE (FINAL) HOST

THE HARBOUR OF ADULT HELMINTH OR SEXUALLY STAGE OF PROTOZOAN.

INTERMEDIATE HOST

THE HARBOUR OF LARVAL HELMINTH OR ASEXUALLY STAGE OF PROTOZOAN, ACCORDING TO PRIORITY THEY ARE CLASSIFIED INTO FIRST, SECOND, THIRD INTERMEDIATE HOST.

RESERVOIR HOST

IS THE VERTEBRATE HOST WHICH HARBOURS THE SAME SPECIES OF PARASITE AS SAME STAGE AS IN A HUMAN HOST. THEY ARE IMPORTANT SOURCES OF INFECTION IN EPIDEMIOLOGY.

• •

THE ANIMAL IS AN NORMAL HOST. THEY CAN CAUSE ZOONOSIS.

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7. ZOONOSIS: REFERS TO ANIMAL’S DISEASES WHICH CAN BE TRANSMITTED TO MAN. (THESE ANIMALS INFECTED WITH PARASITES ARE CALLED RESERVOIR HOSTS. THIS PARASITE IS CALLED PARASITIC ZOONOSES. 8. LARVA MIGRANS－－MEANS THAT WHEN THE LARVAE LIVE IN THEIR ABNORMAL HOST, THEY CAN NOT GROW INTO ADULTS BUT CAN WANDER EVERYWHERE AND CAUSE THE LOCAL OR SYSTEMIC PATHOLOGICAL LESIONS OF THE HOSTS. SUCH AS A LARVAL STAGE OF ASCARIS CANIS IN OUR BODY. 9. PARATENIC HOST (TRANSPORT HOST): IS AN ABNORMAL HOST IN WHICH SOME PARASITIC LARVAE CAN SURVIVE BUT CAN’T DEVELOP INTO THE ADULT STAGE. IF THE LARVAE HAVE A CHANCE TO ENTER THEIR APPROPRIATE HOSTS, THEY CAN CONTINUE TO DEVELOP INTO ADULTS THERE. 10. LIFE CYCLE::

IS THE PROCESS OF A PARASITE’S GROWTH, DEVELOPMENT AND REPRODUCTION, WHICH PROCEEDS IN ONE OR

MORE DIFFERENT HOSTS.

11. INFECTIVE STAGE:: IS A STAGE WHEN A PARASITE CAN INVADE HUMAN BODY AND LIVE IN IT .

12. INFECTIVE ROUTE:: IS THE SPECIFIC ENTRANCE THROUGH WHICH THE PARASITE INVADES THE HUMAN BODY. 13. INFECTIVE MODE:: MEANS HOW THE PARASITE INVADES HUMAN BODY, SUCH AS THE CERCARIAE OF THE BLOOD FLUKE ACTIVELY PENETRATE THE SKIN OF A SWIMMING MAN AND THE INFECTIVE ASCARIS EGGS ARE SWALLOWED BY MAN. 14. ALTERNATION OF GENERATION: IN LIFE CYCLES OF SOME PARASITES, THERE ARE THE REGULAR ALTERNATIONS OF SEXUAL AND ASEXUAL REPRODUCTIONS , THIS PHENOMENON IS CALLED ALTERNATION OF GENERATION, SUCH AS THE LIFE CYCLE OF PLASMODIUM VIVAX.

patient

host carrier

15. CARRIER:: A PERSON WHO HARBOURS PARASITE HAS NO CLINICAL SYMPTOMS, IS AN IMPORTANT SOURCE OF INFECTION IN EPIDEMIOLOGY.THE PARASITE CAN BE DETECTED BY NORMAL EXAMINATION. 16.STERILIZING IMMUNITY: THE IMMUNITY CAN CLEAN UP THE PARASITES IN THE HOST, AND THE HOST WILL FULLY RECOVER FROM THE PARASITOSIS AND NEVER BE INFECTED AGAIN. (SUCH AS THE CUTANEOUS LEISHMANIASIS CAUSED BY LEISHMANIA TROPICA)

17. NON-STERILIZING IMMUNITY: THE IMMUNITY CAN’T CLEAN UP THE PARASITES IN THE HOST, BUT MAY PROTECT THE BODY FROM SUPERINFECTION AS LONG AS THE PARASITES REMAIN IN THE BODY. THIS MAY BE OF GREAT IMPORTANCE IN ENDEMIC AREAS IN LIMITING THE SEVERITY OF INFECTION WITH PLASMODIUM, SCHISTOSOME, HOOKWORMS AND OTHER PARASITES. MCQ 1. THE HOST WHICH CONTAINS ONLY THE IMMATURE STAGES OF A PARASITE IS TERMED THE ......

A. DEFINITIVE HOST B. PARAENTENIC HOST C. INCIDENTAL HOST D. INTERMEDIATE HOST E. ZOONOTIC HOST ANS::

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2. A HOST THAT SIMPLY SERVES TO TRANSPORT A PARASITE FROM ONE HOST TO ANOTHER (I.E. NO DEVELOPMENT OCCURS IN THIS HOST), USUALLY UP THE FOOD CHAIN. A. DEFINITIVE HOST B. PARAENTENIC HOST C. INCIDENTAL HOST D. INTERMEDIATE HOST E. ZOONOTIC HOST ANS::

Chapter 45 LOBOSEA Section 1 Entamoeba histolytica  

The life cycle of E. histolytica is completed in a single host, the man.

Man is the main and probably the only natural host of E. histolytica.

The infective stage: MATURE QUADRINUCLEATE CYST The infective route: ORAL The infective mode: INGESTION Ecological niches: LARGE INTESTINE; LIVER, LUNG & OTHER ORGANS. Pathogenic stage: TROPHOZOITE Diagnostic stage: CYST; TROPHOZOITE

 Life Cycle

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• Cysts of E.histolytica can remain viable and infective in a moist, cool environment for at least 12 days, and in water they can live up to 30 days.

• Cysts are rapidly killed by putrefaction, desiccation, and temptures below -5℃ and above 40℃.

 Pathogenesis and symptomatology A. Pathogenic mechanism a. Asymptomatic infection (carrier) >90% cases b. Symptomatic cases <10% i. 8-10% dysentery, colitis, etc ii. 2% invasive amoebiasis iii. 0.1% deaths  Factors that determine invasion of amebas include the following: o the number of amebas ingested; o the pathogenic capacity of the parasite strain

virulent strain low virulent strain

o host factors such as gut motility and immune competence, and the presence of suitable enteric bacterium that enhance amebic growth.  The sequential stages through which the ameoba invade the large intestine.

1. Adherence of trophozoites on the surface of the large intestine; 2. 2. Invasion of the large intestine; (trophozoits can secrete numerous proteolytic enzymes, et al) 3. 3. Resistance of the amoebae to various effector mechanisms of the host.

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Parasitology Exam Review 2015 B. Pathologic changes  

the characteristic “flask-shaped” ulcer of primary amebiasis “flask-shaped” ulcer------ a small point of entry, leading via a narrow neck through the mucosa into an expanded necrotic area in the submucosa.

C. Symptoms  Asymptomatic infections Carrier ------may have vague and nonspecific abdominal symptoms;  Symptomatic infections (1) Intestinal Amoebiasis Intestinal amoebiasis is the most common form of infection.

Most in the ileocecal junction and colon sigmoideum.  Acute Intestinal Amoebiasis diarrhea or dysentery (with blood, mucus and pus in the stool); abdominal pain and cramping; flatulence, anorexia, weight loss, chronic fatigue.  Chronic Intestinal Amoebiasis alternation of formed stool and loose stool.

(1) Extra-intestinal Amoebiasis Clinical manifestations of extra-intestinal amoebiasis depend upon the organ involved.  Hepatic Amoebiasis （most common extra-intestinal amoebiasis): Non-suppurative amoebic hepatitis------hepatomegaly, right upper quadrant pain, fever and leucocytosis.

Amoebic liver abscess-----fever, sweating, loss of weight and abdominal pain. 

Pulmonary Amoebiasis: o o o

It occurs in 10% ~ 20% of patients.

It is the most common complication of amoebic liver abscess.

May be caused by rupture of a superior right lobe abscess through the diaphragm into the lung parenchyma. o May be caused by the parasites from the colon.

Cough, pleuritic pain and dyspnea are the common clinical manifestations. 

Cerebral Amoebiasis: o Is very unusal. o Is single, small and is located in cerebral hemisphere



Genito-urinary Amoebiasis: o Amoebiasis of the penis is acquired during vaginal or anal intercourse. o In females, rectum-vaginal fistula causes amoebic trophozoites spread to the genito-urinary tract. （ amoebic vaginitis）

 Splenic Amoebiasis: Is caused by transmission of amoebic trophozoites directly through an adherent splenic flexure of intestine.

D. Diagnosis  Clinical diagnosis:: tourist history, the food, dietetic hygiene, abnormal sexual history, etc  Laboratory Diagnosis A. Parasitic Diagnosis

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Parasitology Exam Review 2015 1. Acute Intestinal Amoebiasis patients: sample----liquid stool with blood, mucus and pus method-----wet mount or stained by hematoxylin pathogen----amoebic trophozoits 2. extra-intestinal Amoebiasis: sample----the object sucked from the abscess method----wet mount pathogen-----amoebic trophozoits 3. Carrier: sample----formed stool method-----concerned and stained by iodine fluid or hematoxylin pathogen----cyst • •

The cyst should be carefully differentiated from the non-pathogenic amoebae.

The most common is Entamoeba Coli.

B. Serological Test C. Radio-Imaging Dianosis Ultrasonic B, X ray, CT(Computed Tomography) , MRI(Magnetic Resonance Imaging) E. Prevention: infection is transmitted from one person to another by following ways(route of transmission) 1.

Faecal-Oral route: Ingest the water, vegetable and food contaminated by faeces containing cysts.

2. Vectors: Flies and cockroaches mechanically may transmit cysts from the faeces to the unprotected food and water.

3. Sexual contact It can be sexually transmitted among sexually promiscuous male homosexuals.

The amoebae are transmitted by the sexual practice that allows faecal-oral contact.

F. Treatment The treatment of amoebiasis is broadly based on: ☻ Eradication of amoebae by the use of amoebicides: IODOQUINOL, DILOXANIDE FUROATE, PARAMOMYCIN, METRONIDAZOLE, TINIDAZOLE ☻ Replacement of fluid, electrolyte and blood. ☻ Relief from the constitutional symptoms.

>>>> REVIEW ★ life cycle Parasite site: Colon, liver…

Source: carrier, chronic infection Infective stage : mature cyst ( 4 nuclei) Infective mode: mouth Transmission route: Contaminated water、hand、food、fly、cockroach ★ Pathogenesis and main symptom >Flask-shaped ulcers.

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Parasitology Exam Review 2015 >Intestinal tissue between the two ulcers nearby is almost normal. >If the muscular layer is penetrated -intestinal perforation occur. >Extra-intestinal Amebiasis Diagnosis To find out active trophozoites in the feces or in the ulcer.

1. acute amoebiasis --- bloody-mucous stool ------ active trophozoites 2. carrier--- formed feces --- cyst 3. chronic patients --- feces---- trophozoites or cyst, or find out the typical ulcer in the colon and find out the active trophozoites in granulomatous section.

4. Serological examination Treatment  Eradication: metronidazole  Replacement  Relief

QUESTIONS 1.What’s the infective stage of Entamoeba histolytica? And the infective method?

Ans:: The infective stage: MATURE QUADRINUCLEATE CYST The infective route: ORAL The infective mode: INGESTION Ecological niches: LARGE INTESTINE; LIVER, LUNG & OTHER ORGANS. Pathogenic stage: TROPHOZOITE Diagnostic stage: CYST; TROPHOZOITE

2.What diseases can be caused by Entamoeba histolytica?

Ans :: The diseases that can be caused are: (1) Intestinal Amoebiasis Intestinal amoebiasis is the most common form of infection.

Most in the ileocecal junction and colon sigmoideum.  Acute Intestinal Amoebiasis diarrhea or dysentery (with blood, mucus and pus in the stool); abdominal pain and cramping; flatulence, anorexia, weight loss, chronic fatigue.  Chronic Intestinal Amoebiasis alternation of formed stool and loose stool.

(2) Extra-intestinal Amoebiasis

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Clinical manifestations of extra-intestinal amoebiasis depend upon the organ involved.  Hepatic Amoebiasis （most common extra-intestinal amoebiasis): Non-suppurative amoebic hepatitis------hepatomegaly, right upper quadrant pain, fever and leucocytosis.

Amoebic liver abscess-----fever, sweating, loss of weight and abdominal pain. 

Pulmonary Amoebiasis: o It occurs in 10% ~ 20% of patients. o It is the most common complication of amoebic liver abscess. o May be caused by rupture of a superior right lobe abscess through the diaphragm into the lung parenchyma. o May be caused by the parasites from the colon.

Cough, pleuritic pain and dyspnea are the common clinical manifestations. 

Cerebral Amoebiasis: o Is very unusal. o Is single, small and is located in cerebral hemisphere



Genito-urinary Amoebiasis: o Amoebiasis of the penis is acquired during vaginal or anal intercourse. o In females, rectum-vaginal fistula causes amoebic trophozoites spread to the genito-urinary tract. （ amoebic vaginitis）

 Splenic Amoebiasis: Is caused by transmission of amoebic trophozoites directly through an adherent splenic flexure of intestine.

3.What difference between the identification of the acute intestinal amoebiasis and the chronic?

(1) Intestinal Amoebiasis Intestinal amoebiasis is the most common form of infection.

Most in the ileocecal junction and colon sigmoideum. 

Acute Intestinal Amoebiasis

diarrhea or dysentery (with blood, mucus and pus in the stool); abdominal pain and cramping; flatulence, anorexia, weight loss, chronic fatigue.

 Chronic Intestinal Amoebiasis alternation of formed stool and loose stool.

4. Protozoans utilize all the following types of reproduction except .......... a.multiple fission b.conjugation c.sexual reproduction d.simple binary fission e.all of the types above are used by protozoans Ans:: 5. Risk groups for Entamoeba histolytica include all of the following except ............ a. rural children in the southeastern United States b. homosexual males c. individuals hiking in mountainous areas d. recent world travelers Ans::

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Parasitology Exam Review 2015 6. Identify the true statement. a. b. c. d. e.

Entamoeba coli is a common commensal found in colon Entamoeba histolytica is virtually always pathogenic to it’s host watery, diarrhetic feces that contains Entamoeba histolytica is more infectious to other people than solid feces containing Entamoeba histolytica. if Entamoeba histolytica invades into tissues, the first organ infected tend to be the spleen Entamoeba histolytica only lives in the colonic cavity and the colonic wall tissue.

Ans ::

Chapter 46 ZOOMASTIGOPHOREA Section 1 Trichomonas vaginalis • Location: the vagina in the female and the urethra, epididymis and prostate gland in the male.

• Sources: infected female or male • Transmission route: sexual intercourse, medium, iatrogenic infection, etc.

• Medicine: METRONIDAZOLE 

The LIFE CYCLE includes only one stage---trophozoite.



T. vaginalis reproduces by longitudinal binary fission.



Pathogenesis The factors affecting pathogenicity:  the virulence and number of the parasite strain  the pH and physiologic status of the vaginal and other genitourinary tract surfaces  the accompanying bacterial flora  the integrity of the squamous epithelium of the genitourinary  the optimum pH range for the protozoa to reproduce is approximately 5.0~6.0  the normal vaginal acidity of pH is 3.8~4.4.  Lactobacilli can ferment the glycogen in vaginal epithelia and produce the lactic acid.



Treatment  Oral metronidazole or tinidazole is extremely effective (can cure >95% cases)  Oral metronidazole is not recommended during the first trimester of pregnancy.(may has teratogenic activity)  The patient’s sexual partner should be examined and treated simultaneously.

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 Mechanical protection should be used during intercourse until the infection is eradicated in both partners.

Section 2 Giardia lamblia • • • • • • • • •

Location: duodenum and jejunum Infective stage : mature cyst ( 4 nuclei) Access: mouth Sources: carrier, chronic infection, reservior hosts Infective mode: mouth / ingestion Transmission route: Contaminated water、hand、food、fly、cockroach Disease: diarrhea, cholecystitis or cholangitis Pathogenic stage: trophozoite Diagnostic stage: cyst; trophozoites • Mechanism: A. Pathogenic mechanism G. lamblia is usually weakly pathogenic for humans.  Mechanical blockade of the intestinal mucosa by large numbers of Giardia  Affect the intestinal absorption of nourishment(crypt hypertrophy, villous atrophy or flattening, epithelial cell damage)  Disaccharidase deficiency (fatty diarrhea ) B. Symptoms In endemic situations, over two thirds of infected patients are asymptomatic.  diarrhea is typical. the stool is foul smelling, greasy in appearance, floats on water and without blood or mucus.

Upper abdominal cramping, abdominal distention, flatus.  Cholecystitis or cholangitis  It can become severe in young children and immunocompromised individuals (significant malabsorption, weight loss, malnutrition).

Laboratory diagnosis  The examination of stool The diagnose is made by finding the cyst in formed stool or the trophozoite in diarreal stools. >acutely symptomatic patients------wet mount to find trophozoites. >chronic cases----- cysts may be concentrated by flotation or by sedimentation methods such as the formalin-triton-ether(FIE) method  The examination of duodenal fluid obtained by intubation  the duodenal capsule technique (entero test)  Jejunal biopsy

Treatment  Chemotherapy is generally successful and the risk of side effects is low.  Four drugs are currently available: METRONIDAZOLE, FURAZOLIDONE, QUINACRINE HYDROCHLORIDE & PAROMOMYCIN.

Section 3 Leishmania      

Infective stage: promastigotes Mode of infection: bitten by sandfly Site of habitation: macrophages Pathogenic stage: amastigotes Diagnostic stage: amastigotes Reservoir hosts: dogs [The life cycle need two hosts: vertebrate (human, dog, and other wild animals) and sandfly.]

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Chapter 47 SPOROZOA Section 1 Plasmodia 

Intermediate host : HUMAN



Definitive host : MOSQUITO



Infective stage : SPOROZOITE



Infective mode : MOSQUITO BITE SKIN OF HUMAN



Parasitic position : LIVER AND RED BLOOD CELLS



Transmitted stage : GAMETOCYTES



Schizogonic cycle in red cells: 48 hrs/P.v；



Sporozoite of P.V: TACHYSPOROZITE AND BRADYSPOROZITE

P. VIVAX(P.V)

BENIGN TERTIAN MALARIA

MOST WIDELY DISTRIBUTED OF THE FOUR SPECIES

((PAROXYSM EVERY 2DAYS))

P. FALCIPARUM(P.F)

MALIGNANT TERTIAN MALARIA

THE DOMINANT ORGANISM OF THE TROPICS.

P. MALARIAE(P.M)

QUARTAN MALARIA

RARE AND FOUND PRINCIPALLY IN AFRICA.

P. OVALE(P.O)

TERTIAN MALARIA

FOUND PRIMARILY IN TEMPERATE AND SUBTROPICAL AREAS.

• LIFE CYCLE OF P.V 

Malaria parasite is sporozoa



ALLTERNATION OF GENERATION-----sexual and asexual cycles of reproduction are completed in different host species.



Two hosts: human and mosquito



Vehicle: mosquito

LIFE CYCLE IN HUMAN 1. pre-erythrocytic stage or exoerythrocytic stage(EE) exist in liver cells (hepatocytes)-----schizogony 2. erythrocytic stage （ES） exist in erythrocytes-----schizogony 3. Gametocyte forming stage exist in erythrocytes-----the beginning of the sexual reproduction

LIFE CYCLE IN MOSQUITO Gametogony－－stomach lumen, gamogenesis, sexual reproduction Sporogony－－stomach wall, agamogenesis, asexual reproduction

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LIFE CYCLE OF P.V IN HUMAN 1. pre-erythrocytic stage EE (exo-erythrocytic stage) tachy-sporozoites TS----- 8 days brady-sporozoites BS------6-12months 2. erythrocytic stage (ES) 48h schizogony result in more merozoites 3. Gametocyte forming stage

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GAMETOCYTE PRE-ERYTHROCYTIC STAGE SCHIZOGONIC CYCLE IN RBC: IN ONE SCHIZOGONIC CYCLE: RING FORM

P. VIVAX

P. FALCIPARUM

6 days

CRESCENT SHAPE or SAUSAGE SHAPE 6 days

48 hrs

36-48 hrs

12-24 merozoites

10-36 merozoites

a) CLINICAL MANIFESTATION AND PATHOGENESIS 1. Incubation period: b) Threshold: P.V----10~500/ml; P.F----500~1300/ml exo-erythrocytic stage + many erythrocytic stages c) Factors affect the incubation period the specie, numbers of plasmodium invaded the host, the immunity of host, Chemoprophylaxis, infective route P.v. 14-17 days P.f. 8-12 days d) Infective route :: > Mosquito bite > Blood transfusion e) Paroxysm (attack of malaria) Three stages of each paroxysm (1) The cold stage (chill): lasting for 30min-1hr; fatigue, headache, chill…

(2) The hot stage(fever): lasting for 1-4hr (3) Sweating stage 1-2hr OTHER CLINICAL MANIFESTATIONS a) MALIGNANT TERTIAN MALARIA >Tropical splenomegaly syndrome. >splenomegaly >cerebral malaria caused by P.f. (small vessels are plugged) b) FATAL MALARIA >Cerebral malaria caused by P.f. (small vessels are plugged) c) MALIGNANT MALARIA • Cerebral malaria: delirium , convulsions, paralysis, coma, rapid death.

• Acute respiratory distress syndrome (ARDS): this frequently accompanies cerebra malaria, killing about 80% of those involved.

• Renal failure: • Serious anemia: • Shock

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RECRUDESCENCE AND RELAPSE • Recrudescence occurs when the blood schizonticide does not eliminate all parasites from the blood stream, either because the dose was inadequate or because the parasite is resistant to the drug.

• Rudimental parasites in blood cells • Threshold • Relapse occurs in P.vivax and P.ovale infections after the delayed development of liver-stage parasites that have not been treated adequately with a tissue schizonticide.

• Brady sporozoites • P.f and P.m have only recrudescence, but P.v and P.o both have relapse and recrudescence.  Remnant of parasites in RBC will result in recrudescence.

All the four malaria have RECRUDESCENCE.  Brady sporozoites in liver will cause relapse.

Only P.v and P.o has RELAPSE.

TREATMENT  CHLORQUINE 、QUININE、ARTEMISININ and ARTEMETHER----anti-erythrocytic stage drugs. (question: Which stage of plasmodium can be killed by these drugs ?)  PRIMAQUINE and PYRIMETHAMINE ----anti-exoerythrocytic stage drugs.  PRIMAQUINE (anti-exoerythrocytic & gametocyte)

Pyrimethamin e

Quinine

Chloroquine

Primaquine

Anti-ES

+++

+++

-

-

Anti-EE

-

-

++

++

AntiGametocyt e

-

-

++

++

1. CAN BLOOD TRANSFUSION TRANSMIT MALARIA? ANS: INFECTIVE ROUTE-----

 MOSQUITO BITE  BLOOD TRANSFUSION 2.WHY IS THE ANEMIA DISPROPORTIONATE TO THE DEGREE OF PARASITISM? ANS: MECHANISM:  PARASITIZED ERYTHROCYTES ARE DESTROYED DIRECTLY BY SCHIZOGONY.  PARASITIZED ERYTHROCYTES ARE PHAGOCYTIZED BY A STIMULATED RETICULOENDOTHELIAL SYSTEM  DEPRESSION OF MARROW FUNCTION

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 SEQUESTRATION OF NONPARASITIZED ERYTHROCYTES WITHIN THE ENLARGING SPLEEN 3. WHICH STAGE OF PLASMODIUM CAN BE KILLED BY CHLORQUINE 、QUININE、ARTEMISININ and

ARTEMETHER? ANS :: ANTI-ERYTHROCYTIC STAGE DRUGS.

4.MCQ 1. WHICH DRUG IS EFFECTIVE AGAINST A WIDE RANGE OF INTESTINAL AND OTHER LUMINAL PROTOZOA? A. METRONIDAZOLE B. PENTAMIDINE C. ANTIMONIALS D. 4-AMINOQUINOLINES ANS:: 2. WHICH OF THE FOLLOWING INTESTINAL INFECTIONS WOULD YOU FIRST CONSIDER IF THE SYMPTOMS INCLUDED DYSENTERY AND CRAMPS?

A. ENTAMOEBA HISTOLYTICA B. LEISHMANIA DONOVANI C. GIARDIA LAMBLIA D. CRYPTOSPORIDIUM HOMINIS ANS:: 3. DETECTION OF AMASTIGOTES FROM SCRAPINGS OR ASPIRATES OF A CUTANEOUS LESION IS DIAGNOSTIC OF _______.

A. AMOEBIASIS B. LEISHMANIASIS C. AFRICAN TRYPANOSOMIASIS D. EITHER AMOEBIASIS OR LEISHMANIASIS SINCE AMASTIGOTES CANNOT BE DISTINGUISHED ANS::

Section 2 Toxoplasma gondii • The infective stage: OOCYST, TISSUE CYST, TRAPHOZOITE; • The infective route: BY MOUTH, BY WOUNDED SKIN OR MUCOSA, BY PLACENTA,

BY BLOOD TRANSFUSION OR ORGAN TRANSPLANTATION; • The intermediate host: HUMAN, ANIMALS; • The definitive host: THE CAT AND OTHER FELIDS

TREATMENT • Drugs are effective against tachyzoites.

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• • •

PYRIMETHAMINE, SULFADIAZINE and CLINDAMYCIN Cerebral toxoplasmosis-----AZITHROMYCIN Pregnant patients-----SPIRAMYCIN

TERMS 1. OPPORTUNISTIC PARASITE :: THE PARASITE IN AN IMMUNOCOMPETENT HOST IS LOW VIRULENCE THAT SELDOM PRODUCES DISEASE, AND CAN’T BE DETECTED BY NORMAL EXAMINATION（SUPPRESSIVE INFECTION). BUT INFECTION IN AN IMMUNOCOMPROMISED (SUCH AS AIDS…) HOST MAY BE MANIFESTED BY SEVERE DISEASE, SOMETIMES BE LETHAL.

Section 3 Cryptosporidium IT CAN CAUSE CRYPTOSPORIDIOSIS WHICH RESULTING IN DIARRHEA AND THE MOST SEVERE INFECTIONS IN IMMUNECOMPROMISED INDIVIDUALS

Treatment • No specific and effective antimicrobial agent for cryptosporidiosis are available.

• PAROMOMYCIN is applied in treating cryptosporidiosis recently, and may prevent relapse when be given orally. It’s also used for amoeba, gram-negative bacterium, tapeworm infection.

• LETRAZURIL can improve symptoms in 40% of patients.

• AZITHROMYCIN is available for pediatric patients.

•

NITAZOXANIDE is a new drug.

17

mature quadrinucleate cyst

Trophozoite

mature quadrinucleate cyst

Promastigote

Pseudocyst, tissue cyst, oocyst

Oocyst

TRICHOMONAS VAGINALIS

GIARDIA LAMBLIA

LEISHMANIA DONOVANI

TOXOPLASMA GONDII

CRYPTOSPORIDI UM

INFECTIVE STAGE

ENTAMOEBA HISTOLYTICA

PARASITE

Ingestion

Ingestion, skin or mucosa wounds, placenta

Bite of sandfly

ingestion

Intercouse and touch

Ingestion

INFECTIVE ROUTE

No

No

Bite of sandfly

Stool, bile

Vaginal discharge or urine or semen

Stool

DISCHARGE

Small intestinal

Stool

Definitive host---stooll

Nucleated cells ntermediate host----can’t be discharged;

Macrophage (in liver, spleen, lymph node, bone marrow)

Duodenum, gallbladder or bile duct

No

No

Vagina, urethra, prostate

large intestine; liver, lung and other organs

INHABITATION

No

No

MIGRATI ON

Diarrhea(flattened and fused small intestinal villi…)

Congenital toxoplasmosis, acquired toxoplasmosis

Fever, slenomegaly, hepatomegaly, lymphadenectasis

Diarrhea, cholecystitis or cholangiolitis

Vaginitis, Urethritis, Prostatitis

Diarrhea, liver abscess

HARMS

Stool examination

Print slide or smear slide(lymphnode, blood, cerebrospinal fluid)

Smear

Wet mount of stool or Duodenal juice

Wet mount

Chronic—stained with iodine fluid

Acute--wet mount;

DIAGNOSE METHODS

Parasitology Exam Review 2015 18

Parasitology Exam Review 2015

The important points for all human parasites we learned 1. Life cycle; 2. pathogenic mechanism and Clinical manifestations; 3. the best method of pathogenic diagnosis; 4. best drugs for different parasites: nematode (Albendazole), trematode (Praziquantel ), cestode (Praziquantel ) Filaria (DEC, or Hetrazan ).

Chapter 49 TREMATODES Section 1 Introduction 1.C OMMON FEATURES OF ADULT a) Most adult trematodes are dorsoventrally flattened, bilaterally symmetric, leaf-shaped or tongue-like. b) All of them have two suckers, an oral and a ventral sucker. c) The reproductive system is developed and hermaphroditic.

2. FEATURES OF LIFE CYCLE

2. ALTERNATION OF GENERATIONS IS PRESENT IN THEIR LIFE CYCLES. 3. THEY ARE BIOHELMINTHS. 4.EGGS DEVELOP ONLY AFTER GETTING INTO FRESH WATER. 5. THEIR INTERMEDIATE HOSTS ARE IN WATER. 1ST INTERMEDIATE HOSTS ARE ALL SNAILS. 6. INFETIVE STAGE IS USUALLY A METACERCRIA 7. THEY HAVE THEIR RESERVOIR HOSTS. THE FLUKE DISEASES ARE ZOONOSES.

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Parasitology Exam Review 2015

Section 2 Clonorchis sinensis (LIVER FLUKE) PPT REVIEW QUESTIONS 1. WHAT ARE THE PATHOGENESIS AND SYMPTOMS OF LIVER FLUKE？ 2. WHAT ARE THE LIFE CYCLE FEATURES OF LIVER FLUKE ?

PPT REVIEW SOLUTIONS 1. PATHOGENESIS  1. MECHANICAL LESION OF ADULT WORMS: CAUSING EROSION OF THE EPITHELIUM OF BILE DUCTS.  2. HYPERSENSITIVITY AND INFLAMMATION: INDUCING ENLARGEMENT OF LOCAL BILE DUCT, AND PROLIFERATION OF BILIARY EPITHELIUM → BILIARY EPITHELIUM FALLEN OFF, EPITHELIAL HYPERPLASIA →ADENOMA→ BILE STREAM BLOCKAGE.

 3. BILE STREAM BLOCKAGE→BACTERIAL COINFECTION, CAUSING CHOLECYSTITIS, CHOLANGITIS AND CHOLELITHIASIS.  4. BILE STREAM BLOCKAGE, BILE IS STORED INCREASINGLY IN LIVER: CAUSING DEGENERATION AND NECROSIS OF LOCAL HEPATIC CELLS → BILIARY CIRRHOSIS → PORTAL VEIN HYPERTENSION, FUNCTION FAILURE → ASCITES, HEPATOMEGALY, ANEMIA, COMA OR LIVER CANCER → DIE. SYMPTOMS • THE MOST COMMON LESION IS INVOLVED IN LIVER. > LIGHT INFECTION: NO SYMPTOMS. (1) ACUTE STAGE: FEVER, GASTROINTESTINAL DISCOMFORT, ABDOMINAL DISTENSION, WEAKNESS OF LIMBS, HEPATIC PAIN, EOSINOPHILIA. (2) CHRONIC STAGE: > GENERAL CASE: POOR APPETITE, DIARRHEA, PHYSICAL WEAKNESS, HEPATIC PAIN. > BACTERIAL COINFECTION: CAUSING CHOLECYSTITIS, CHOLANGITIS AND CHOLELITHIASIS. SEVERE CASE: JAUNDICE, TOXEMIA, CHILL, FEVER, VOMITING, VERTIGO, MENTAL DISORDER, EMACIATION, HEMORRHAGE OF UPPER PART OF DIGESTIVE TRACT. VERY SEVERE CASE: ASCITES, HEPATOMEGALY, ANEMIA, COMA OR LIVER CANCER, EVEN DEATH. IN CHILD CASE: RETARDED GROWTHS (DWARF) IN BOTH OF PHYSICAL AND MENTAL .

EASILY MISDIAGNOSED AS HEPATITIS, CHRONIC CHOLECYSTITIS, ETC 2.LIFE CYCLE FEATURES OF LIVER FLUKE 1. INFECTIVE STAGE: METACERCARIA; 2. INFECTIVE ROUTE AND MODE: EATING RAW OR UNDERCOOKED FRESH WATER FISH AND SHRIMPS WITH METACERCARIAE; 3. SITE OF INHABITATION: BILE DUCTS; 4. BIOHELMINTH: 1ST INT. HOSTS: BITHYNIA SNAIL; 2ND INT. HOSTS: FRESHWATER FISH, SHRIMP 5. RESERVOIR HOSTS: CAT, DOG; 6. LIFE SPAN: 20-30 YEARS

Section 3 Paragonimus spp (LUNG FLUKE) PPT QUESTIONS 1. WHAT ARE THE PATHOGENESIS AND SYMPTOMS OF LUNG FLUKE？ ANS : > PATHOGENESIS AFTER EXCYSTATION, THE ADOLESCENTS PENETRATE THE INTESTINAL WALL AND MIGRATE TO THE LUNGS OR OTHER ORGANS, CAUSING LESION. 1. ACUTE STAGE: LARVAL MIGRATION→ INTO DIFFERENT ORGANS AND TISSUES→ INDUCE LOCALIZED INFLAMMATION→ HEMORRHAGE, PURULENCY. 2. CHRONIC STAGE: CLASSIFIED INTO 3 STAGES: (1) ABSCESS STAGE: ADULTS PRESENCE→ INFLAMMATION →TISSUE DAMAGE, BLEEDING→ INFILTRATION OF NEUTROPHILS AND EOSINOPHILS SURROUNDING FOCUS OF INFECTION, TO FORM GRANULATION TISSUE→ CAPSULE WALL. (2) STAGE OF FIBROUS CYST: EXUDATIVE INFLAMMATION → CHOCOLATE OR RUSTY THICK FLUID WITH EGGS AND CHARCOT-LEYDEN CRYSTALS WITHIN CYST. IN THIS STAGE, THE SHADOW OF THE CYST CAN BE SEEN ON X-RAY. PATIENTS COUGH OUT THE RUSTY SPUTUM WHEN THE CYST ERODES BRONCHIOLES. (3) FIBER SCAR STAGE: THE WORMS ARE DEAD OR ESCAPE FROM THE CYST→ CAPSULE CONTENTS ARE EXPELLED OR ABSORBED→GRANULATION TISSUE FILLING →FIBROSIS→SCAR.

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Parasitology Exam Review 2015 2. WHAT ARE THE LIFE CYCLE FEATURES OF LUNG FLUKE? 1. Infective stage: METACERCARIAE 2. Infective mode: EATING RAW FRESH WATER CRABS AND CRAYFISH WITH METACERCARIAE 3. Infective route: BY MOUTH INGEST 4. Site of inhabitation: LUNG AND OTHERS 5. Intermediate hosts: 1st int. host is melania snail 2nd int. hosts are crab and crayfish 6. Reservoir hosts: CARNIVORES SUCH AS TIGER, LION, WOLF, FOX, DOG, CAT. 7. Life span: 5-6 years, even up to 20 years 8.Ectopic parasitism: BRAIN, LIVER, PANCREAS, KIDNEY, SKELETAL MUSCLE, SUBCUTANEOUS TISSUE. 9. Paratenic host or transport host: PIG, RABIT , WILD BOAR 3.CLINICAL MANIFESTATION OF LUNG FLUKE ?

1. ACUTE STAGE: LIGHT CASE: LOSS OF APPETITE, ABDOMINAL PAIN, DIARRHEA, LOW FEVER; SEVERE SYMPTOM: URTICARIA, HIGH FEVER, CHEST PAIN, COUGH, HEPATOMEGALY. NONSPECIFIC SYMPTOMS, 1-3 MONTHS 2. CHRONIC STAGE: (1) PULMONARY TYPE: THE SYMPTOMS RESEMBLE PULMONARY TUBERCULOSIS (PNEUMONIA) WITH LOW FEVER, COUGH WITH RUSTY SPUTUM AND CHEST PAIN. (2) BRAIN-SPINAL CORD TYPE: EPILEPSY, MONOPLEGIA, APHASIA, VISUAL LESION, RESEMBLES CEREBRAL CYSTICERCOSIS. (3)ABDOMINAL TYPE: ABDOMINAL PAIN，DIARRHEA WITH BLOOD (4)SUBCUTANEOUS TYPE: THE WANDERING AND PAINLESS SUBCUTANEOUS NODULES.

Section 4 Schistosoma japonicum (BLOOD FLUKE) PPT BACK QUESTIONS 1. WHAT’S THE DIFFERENCES BETWEEN BLOOD FLUKE AND OTHER FLUKES? 2. THE ADULTS OF S. JAPONUCUM INHABIT IN MESENTERIC VEIN AND LAY EGGS IN INFERIOR MESENTERIC VEIN SYSTEM， WHY CAN ITS EGGS DISCHARGE IN FECES？

> Feature of Life cycle for blood fluke： 1. Site of inhabitation: MESENTERIC VEIN. 2. Infective stage: CERCARIA 3. Infective route: BY SKIN 4. Intermediate hosts: ONCOMELANIA SNAIL 5. Reservoir hosts: MAMMALS SUCH AS BUFFALO, CATTLE, PIG, GOAT, MONKEY, FOX. 6. Eggs are inlaid in the liver and intestinal wall. Some of them are discharged in feces to complete its life cycle 7. There was NO REDIAE AND METACERCARIA in its life cycle.

SOLUTION FOR PPT BACK QUESTION 1. THE BLOOD FLUKE DIFFERS FROM OTHER FLUKES FROM THE FOLLOWING ASPECTS :: (1) THE ADULT WORMS LOOK LIKE NEMATODES, ELONGATED CYLINDRICAL IN SHAPE. (2) TWO SEXES ARE SEPARATE. (3) EGG WITHOUT OPERCULUM, BUT WITH A LATERAL SPINE. (4) ONLY ONE INTERMEDIATE HOST REQUIRED. (5) THE INFECTIVE STAGE IS CERCARIA. (6) THE INFECTIVE ROUTE IS BY SKIN. (7) THE EGGS ARE MAIN PATHOGENIC STAGE.

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Parasitology Exam Review 2015 2. Site of inhabitation mesenteric vein

Mechanism of Passage to host feces

The mechanism that how the eggs are passed to the outside: >The SEA secreted by the mature eggs. >IV allergy granulomas. >The intestine tissue get inflamed and necrosis. >Enterokinesia, Intraabdominal pressure. >The eggs rupture into the lumen of the bowel

REVIEW BY TEACHER 1.LIFE CYCLE OF BLOOD FLUKE.

2.PATHOGENIC MECHANISM AND CLINICAL MANIFESTATION OF BLOOD FLUKE PATHOGENIC MECHANISM 1) THE PRIMARY LESION IN SCHISTOSOMIASIS IS IMMUNOPATHOLOGY. 2) DIFFERENT STAGES CAN DAMAGE THE HOST, WHICH IS INVOLVED TO HYPERSENSITIVITY (TYPEⅠ, Ⅲ AND Ⅳ TAKE PLACE ).

(1) DUE TO THE CERCARIA WHEN HUMAN SCHISTOSOME CERCARIA REPEATEDLY PENETRATE THE HUMAN SKIN, ALLERGY I AND IV TAKES PLACE. THE CERCARIAL DERMATITIS APPEARS: ITCH, LOCAL EDEMA AND RASHES (2) DUE TO SCHISTOSOMULUM THE MIGRATION OF THE ADOLESCENTS MAY INDUCE LOCALIZED PNEUMONITIS AND URTICARIA. (3) DUE TO ADULTS: MECHANICAL EFFECT AND TOXIC EFFECT OF METABOLITES MESENTERIC PHLEBITIS, HEPATITIS, ABDOMINAL PAIN (4) ***DUE TO EGG >THE MOST SERIOUS DAMAGE IS DONE BY EGGS. COLON AND LIVER ARE MOST SERIOUSLY INVOLVED. >DELAYED TYPE HYPERSENSITIVITY (DTH) REACTION AROUND THE EGG AND FORMATION OF GRANULOMA. CLINICAL MANIFESTATION THERE ARE THREE MAJOR CLINICOPATHOLOGIC STAGES IN SCHISTOSOMIASIS: (1) INITIAL PHASE: > THE CERCARIAL DERMATITIS APPEARS: ITCH, LOCAL EDEMA AND RASHES. IT IS DUE TO CERCARIA PENETRATION FROM SKIN, CAUSING ALLERGY I AND IV. THE SYMPTOMS USUALLY DISAPPEAR AFTER 4 DAYS. >THEN, PNEUMONITIS APPEARS: DRY COUGH, FEVER, URTICARIA. IT IS DUE TO ADOLESCENTS MIGRATION AND ALLERGIC REACTION CAUSING BY EXCRETION MATERIALS FROM ADOLESCENTS . *(2) ACUTE STAGE: >DYSENTERY: THE PATIENT MAY PASS STOOL WITH BLOOD, PUS AND MUCUS 5-10 TIMES PER DAY, IN WHICH A LARGE NUMBER OF EGGS CAN BE

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Parasitology Exam Review 2015 FOUND. >OTHER SYMPTOMS : CHILL, FEVER, AND MALAISE. *(3) CHRONIC STAGE: >CHIEF MANIFESTATION OF THE PATIENTS ARE INTERVAL DIARRHEA. >THE PATIENTS EXPERIENCE FATIGUE, LOSS OF WEIGHT , SPLEEN & LIVER ENLARGEMENT, ANEMIA. >RETARDATION OF BOTH PHYSICAL AND MENTAL GROWTH IN CHILDREN. >MENOPAUSE, STERILITY AND ABORTION MAY OCCUR IN WOMEN. >THIS STAGE MAY LAST FROM SEVERAL YEARS TO 20 YEARS. (4)TERMINAL STAGE OF SCHISTOSOMIASIS：  ※LIVER CIRRHOSIS IS THE PROMINENT SYNDROME OF THIS STAGE. ACCORDING TO THE MANIFESTATIONS, TERMINAL STAGE OF SCHISTOSOMIASIS CAN BE DIVIDED INTO FOUR TYPES:  ①GIANT LIVER AND SPLEEN, ②ASCITES, ③DWARF ④ INTESTINAL CANCROID CHANGE (5) ECTOPIC LESION  SCHISTOSOMIASIS IN LUNGS: FOUND IN ACUTE SCHISTOSOMIASIS, BY EGG DEPOSITION. SYMPTOMS ARE LIGHT AND SIGNS ARE NOT CLEAR.  SCHISTOSOMIASIS IN BRAIN: ACUTE TYPE: CEPHALOMENINGITIS ： IN PATHOLOGY, INFLAMMATION OF THE MEMBRANES OF THE BRAIN: DISTINGUISHED FROM SPINAL MENINGITIS. CHRONIC TYPE: FOCAL EPILEPSY： EPILEPSY IN WHICH THE ATTACKS BEGINS WITH AN ISOLATED DISTURBANCE OF CEREBRAL FUNCTION (AS A TWITCHING OF A LIMB OR AN ILLUSORY SENSATION OR A MENTAL DISTURBANCE).

2.DIAGONISTIC METHOD OF BLOOD FLUKE THE PRESUMPTIVE DIAGNOSIS: * SYMPTOMS * HISTORY OF LIVING IN ENDEMIC AREAS THE DEFINITIVE DIAGNOSIS: DEPENDS ON THE PATHOGEN EXAMINATION AS FOLLOWING: 1. STOOL EXAMINATION (1) DIRECT FECAL SMEAR FOR ACUTE STAGE (2) WATER SEDIMENTATION METHOD AND MIRACIDIA HATCHING TEST: THIS IS THE BEST METHOD 2. BIOPSY CAN BE DONE BY PROCTOSCOPE FOR TERMINAL STAGE OF DISEASE. 3. IMMUNOLOGICAL TESTS ARE SUBSIDIARY FOR REFERENCE ONLY.  IDT (INTRADERMAL TEST)  COPT (CIRCUMOVAL PRECIPITATION TEST)  ELISA（ ENZYME-LINKED IMMUNOSORBENT ASSAY ）IHA（ INDIRECT HEMAGGLUTINATION TEST ）  MONOCLONAL ANTIBODY TECHNIQUE, ETC. 4. IMAGING TEST  B-ULTRASOUND: THE DEGREE OF LIVER CIRRHOSIS  CT: THE IMAGE OF LIVER AND BRAIN  X-RAY: CHEST, ESOPHAGUS, AND GASTROINTESTINAL TRACT

Section 5 Fasciolopsis buski (INTESTINAL FLUKE) 1.LIFE CYCLE OF FASCIOLOPSIS BUSKI 2. MAIN CLINICAL MANIFESTATIONS OF FASCIOLOPSIASIS 3.THE BEST METHOD OF PATHOGENIC DIAGNOSIS FOR FASCIOLOPSIS BUSKI PPT BACK QUESTIONS 1Life cycle of Fasciolopsis Buski 2. Main clinical manifestations of fasciolopsiasis 3. The best method of etiological diagnosis for Fasciolopsis Buski SOLUTION FOR IMPORTANT REVIEW

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Parasitology Exam Review 2015 1. LIFE CYCLE OF FASCIOLOPSIS BUSKI

1. Site of inhabitation: SMALL INTESTINE 2. Infective stage: METACERCARIA 3. Infective mode: EATING RAW WATER PLANTS WITH METACERCARIAE 4. Medium of water plants: WATER CHESTNUT, WATER BAMBOO AND WATER CALTROP, WATER GRASS 5. Intermediate hosts: PLANORBIS SNAIL 6. Reservoir host: PIG 7. definitive host: HUMAN, PIG

2. PATHOGENIC MECHANISM AND CLINICAL MANIFESTATIONS OF INTESTINAL FLUKE > Pathogenesis 1. Mechanical injury：abdominal pain and intestinal disorder.

2. Take nourishment：covering the wall of intestine to affect absorption, causing malnutrition.

3. Allergy: caused by secretions and excrements.

4. Intestinal obstruction: caused by a mass of the worms, occasionally.  Clinical Manifestation 1. Light infection: no symptom (most cases).

2. Heavier infections: diarrhea, abdominal pain, malnutrition, nausea, vomiting, fever.

Occasionally: ascites and intestinal obstruction.

2. MAIN CLINICAL MANIFESTATIONS OF FASCIOLOPSIASIS  Clinical Manifestation 1. Light infection: no symptom (most cases).

2. Heavier infections: diarrhea, abdominal pain, malnutrition, nausea, vomiting, fever.

Occasionally: ascites and intestinal obstruction.

3. THE BEST METHOD OF PATHOGENIC DIAGNOSIS FOR FASCIOLOPSIS BUSKI 1. STOOL EXAMINATION: TO FIND EGGS WITH MICROSCOPY : DIRECT FECAL SMEAR WATER SEDIMENTATION METHOD + FECAL SMEAR 2. VOMITUS OF PATIENT: FIND THE ADULTS BY EYES (RARELY).

REVIEW QUESTIONS FOR TREMATODES 1. WHAT’S THE DIFFERENCES BETWEEN BLOOD FLUKE AND OTHER FLUKES? 2. THE ADULTS OF S. JAPONUCUM INHABIT IN MESENTERIC VEIN AND LAY EGGS IN INFERIOR PORTAL VEIN SYSTEM， WHY CAN ITS EGGS DISCHARGE IN FECES？

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Parasitology Exam Review 2015

Chapter 50 CESTODES Section 1 Introduction of cestodes 1.FEATURES OF LIFE CYCLE IN CESTODES 2. MAIN PATHOGENIC MECHANISM AND CLINICAL MANIFESTATIONS OF CESTODE 3.DIFFERENCES IN MORPHOLOGY AND CLINICAL MANIFESTATIONS BETWEEN T. SOLIUM AND T. SAGINATA SOLUTIONS

1) COMMON FEATURES OF CESTODES :: 1）flattened 2）ribbon-like 3）consisting of proglottids 4）with no digestive tract , mouth and body cavity ； 5） monoecism 6) The body is composed of a head, neck and segmented strobilus 2) CHARACTERISTICS OF CESTODE’S LIFE :: 1)

The adult worm lives in the small intestine of humans or mammals(final host)

2) Tapeworms usually require 1 or 2 intermediate hosts in the life cycle.

3.DIFFERENCES IN MORPHOLOGY AND CLINICAL MANIFESTATIONS BETWEEN T. SOLIUM AND T. SAGINATA Adult T. solium length 2-4 meters scolex 1mm in diameter with 4 suckers and hooklets Number of segment 700 to 1000 Mature proglottid 3 lobes of ovary Gravid proglottid 7-13 uterine lateral branches on one side Number of gravid usually several segments proglottid detached Mode of proglottids passively expelled passing out Cysticercus scolex with hooklets found in man and pig Disease caused in taeniasis and cysticercosis man

T. saginata 4-8 meters 2mm in diameter, with 4 suckers but no hooklets 1000 to 2000 2 lobes of ovary 15-30 uterine lateral branches on one side usually single segment actively migrate out of anus no hooklets on scolex only found in cattle Taeniasis

4. TAENIA SOLIUM AND TAENIA SAGINATA, WHICH IS MORE SERIOUS THAN THE OTHER? WHY? Taenia solium is more serious than Taenis Sagnita because the clinical consequences of tapeworm infections depends on whether the patient serves as p rimary and intermediate host.

In case of Taenia Saginata the human act as primary host and the adult is confined to the lumnen of the gut and thus the consequences of the infection are typically minor. While in case of Taenia Solium the human serves both as primary and intermediate host so the adult cause lesions the lumen of small intestine and the larval development causes tissue invasions in different organs of the body and frequently leading to serious diseases.

25

Parasitology Exam Review 2015

Section 2 Taenia solium, 1.FEATURES OF LIFE CYCLE OF T.SOLIUM

1.

2.

3.

4.

5.

6.

FINAL HOST: HUMAN,

INTERMEDIATE HOST: PIG ;HUMAN INFECTIVE STAGE: CYSTICERCUS ,EGG INFECTIVE MODE: EATING RAW OR UNDERCOOKED PORK ,EATING EGGS SITE OF INHABITATION: ADULT IN SMALL INTESTINE; CYSTICERCUS IN TISSUES, LIFE SPAN: ADULT CAN SURVIVES MORE THAN 25 YEARS (CYSTICERCUS : 5-6 YEARS )

IN HUMAN BODY.

2.PATHOGENIC AND CLINICAL MANIFESTATION 1. MECHANICAL EFFECT OF PARASITES ON HOST INTESTINE 2. DEPRIVING THE HOST OF NOURISHMENT: 3. IMMUNO-PATHOLOGICAL LESION: THE MAJORITY OF CASES ARE SYMPTOMLESS. 1. TAENIASIS (CAUSED BY THE ADULT ): IN SOME PATIENTS THERE MAY BE VAGUE INTESTINAL DISCOMFORT, VOMITING OR DIARRHEA. APPENDICITIS DUE TO THE ENTRY OF SEGMENT INTO THE LUMEN OF THE APPENDIX. INTESTINAL OBSTRUCTION DUE TO GROWTH OF A MASS OF WORMS. 2. CYSTICERCOSIS (CAUSED BY THE CYSTICERCUS ): THE MANIFESTATIONS VARY WITH THE NUMBER OF CYSTICERCI AND THE TISSUES AND ORGANS INVOLVED. THERE ARE THREE TYPES OF CYSTICERCOSIS.

Section 3 Taenia saginata 1)FEATURES OF LIFE CYCLE OF T. SAGINATA 1. FINAL HOST: MAN, 2. INTERMEDIATE HOST: CATTLE 3. INFECTIVE STAGE: CYSTICERCUS, 4. INFECTIVE MODE: EATING RAW OR UNDERCOOKED INFECTED BEEF, 5. SITE OF INHABITATION: IN SMALL INTESTINE， 6. DISEASE CAUSED IN MAN ：JUST TAENIASIS; 7.LIFE SPAN: ABOUT 20~30 YEARS. 8. CATTLE BECOME INFECTED BY INGESTING VEGETATION CONTAMINATED WITH EGGS OR GRAVID PROGLOTTIDS. 2)PATHOGENESIS AND CLINICAL FEATURES OF T.SAGINATA Usually only single worm is present。 The majority of cases are symptomless.

1. taeniasis: Some patients may complain of migrating proglottids from anus with pruritus at the perianal region.

2. Abdominal discomfort, nausea, vomiting, constipation or diarrhea may occur.

3. Appendicitis due to the entry of a segment into the lumen of appendix。 4. intestinal obstruction due to enlargement of a mass of worms.

Section 4 Echinococcus granulosus 1. PATHOGENESIS AND CLINICAL FEATURES OF HYDATIDOSIS PATHOGENESIS 1. MECHANICAL DAMAGE: THE EARLY STAGE OF INFECTION IS GENERALLY ASYMPTOMATIC. AS THE CYST ENLARGES, SYMPTOMS OF A SPACE-OCCUPYING LESION DEVELOP.

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Parasitology Exam Review 2015 2. SECONDARY INFECTION: THE RUPTURE OF CYST WILL CAUSE THE ESCAPE OF HYDATID SAND, AND SCOLICES CAN FORM NEW HYDATID CYSTS IN THE DIFFERENT ORGANS. 3. ALLERGIC REACTION & POISONING : URTICARIA OCCUR FOR THE HYDATID FLUID FROM EXUDATION OR CYST RUPTURED. ESPECIAL DANGEROUSLY, ALLERGIC SHOCK WILL OCCUR, IF THE FLUID FLOW INTO BLOOD CIRCULATION. CLINICAL MANIFESTATION

 ECHINOCOCCUS GRANULOSUS INFECTIONS REMAIN SILENT FOR YEARS BEFORE THE ENLARGING CYSTS CAUSE SYMPTOMS IN THE AFFECTED ORGANS .  THE CLINICAL MANIFESTATION DEPENDS ON THE NUMBER, SITE, AND GROWTH RATE OF CYSTS.  IN MOST OF THE SITUATION, THE DAMAGED ORGANS ARE INVOLVED IN THE LIVER, LUNG. 1. IF THE LIVER IS INVOLVED, IT TENDS TO BECOME ENLARGED. THE CYST PRESENTS AS A PALPABLE HEPATOMEGALY, AND BILIARY DUCT OBSTRUCTION. ABOUT 70% OF THE CYSTS ARE FOUND IN THE LIVER. 2.PULMONARY INVOLVEMENT CAN PRODUCE CHEST PAIN, COUGH, AND HEMOPTYSIS. ABOUT 20% OF THE CYSTS ARE FOUND IN THE LUNG. 3. ABOUT 10% OF THE CYSTS ARE FOUND IN BRAIN, BONE, HEART AND OTHERS, RESULTING SYMPTOMS. IN BRAIN: LIKE THE PATIENTS WITH TUMOR; IN BONE: CAUSING THE BONE FRACTURE EASILY 4.RUPTURE OF THE CYSTS CAN PRODUCE FEVER, URTICARIA, EOSINOPHILIA, AND ALLERGIC SHOCK ( HYDATID SAND DISSEMINATION, HYDATID FLUID FLOW INTO DIFFERENT PLACES.) 2. WHAT ARE CHARACTERISTICS OF LIFE CYCLE OF ECHINOCOCCUS GRANULOSUS

(1) EGGS IS PASSED IN FECES AND EATEN BY HERBIVORES OR HUMANS. (2) ONCOSPHERE PENETRATES GUT WALL AND IS CARRIED TO LIVER(70%), LUNGS(22%) AND OTHER TISSUES BY BLOOD CIRCULATION，TO FORM HYDATID CYSTS IN THESE ORGANS. (3)HYDATID CYSTS FORM IN ORGANS OF INTERMEDIATE HOST (THE HERBIVORES OR HUMAN), CAUSES ECHINOCOCCOSIS. (4) AFTER INGESTION BY CANID, HYDATID CYST IS DIGESTED AND PROTOSCOLEX EVAGINATES. SCOLEX ATTACHES TO INTESTINAL WALL AND DEVELOPS STROBILA (TO FORM AN ADULT).

3. HOW TO CONFIRM HYDATIDOSIS ?

DIAGONSIS 1. IMAGE TEST FLUID FROM A HYDATID CYST WILL SHOWS MULTIPLE PROTOSCOLICES (SIZE APPROXIMATELY 100 µM), EACH OF WHICH HAS TYPICAL HOOKLETS. THE PROTOSCOLICES ARE NORMALLY INVAGINATED (LEFT), AND EVAGINATED (MIDDLE, THEN RIGHT) WHEN PUT IN BRINE SOLUTION. 2. X-RAY, CT EXAMINATION AND VARIOUS ULTRASOUND PROCEDURES MAY REVEAL AND LOCATE THE CYSTS. 3. IMMUNOLOGICAL TESTS: > INDIRECT HEMAGGLUTINATION (IHA), > INDIRECT FLUORESCENT ANTIBODY (IFA) TESTS, > ENZYME IMMUNOASSAYS (EIA) 4.SURGICAL EXAMINATION: TO CONFIRM HYDATIDOSIS THE DIAGNOSIS MAY BE CONFIRMED BY SURGICAL EXAMINATION OF HYDATID CYST，FINDING PROTOSCOLICES. 4. HOW TO PREVENT FROM HYDATIDOSIS? 1) PREVENTING DOGS FROM DIGEST RAW OFFAL AND DEAD ANIMALS. 2) AVOIDING HUMAN CLOSE CONTACT WITH DOGS, CATS AND OTHER CARNIVORES. 3) AVOID EATING RAW VEGETABLES OR FOOD CONTAMINATING WITH DOG FECES.

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Parasitology Exam Review 2015 4) PERSONS LIVING IN ENDEMIC AREAS (PASTURING AREA ) AND THOSE WHO HAVE CONTACT WITH DOGS SHOULD BE PERIODICALLY EXAMINED BY SEROLOGICAL METHODS FOR ANTIBODIES. QUESTIONS FROM PPT 1. WHAT ARE CHARACTERISTICS OF LIFE CYCLE OF ECHINOCOCCUS GRANULOSUS 2. WHAT ARE THE PATHOGENESIS AND CLINICAL FEATURES OF HYDATIDOSIS? 3. HOW TO CONFIRM HYDATIDOSIS ?

4. HOW TO PREVENT FROM HYDATIDOSIS?

Chapter 51 NEMATODA Section 1 Introduction of Nematoda Section 2 Ascaris 1、LIFE CYCLE ( ESPECIALLY BLOOD -LUNG MIGRATION IN LARVE STAGE) ；PULMONITIS 2、COMPLICATIONS FOR BORING HABIT OF ADULT SMALL EXAM QUES:: 1. PLEASE DESCRIBE THE LIFE CYCLE OF ASCARIS, AND PRESENT BRIEFLY THE CLINICAL MANIFESTATIONS OF ASCARIASIS .

SOLUTION FOR IMPORTANT REVIEW

1. CHARACTERISTICS OF ASCARIS LIFE CYCLE 1. SITE OF INHABITATION: UPPER PART OF SMALL INTESTINE 2. INFECTIVE STAGE: EMBRYONATED EGGS 3. ROUTE OF INFECTION: BY MOUTH 4. NO INTERMEDIATE AND RESERVOIR HOSTS 5. LIFE SPAN OF THE ADULT: ABOUT 1 YEAR

1. egg 2. larva 3. adult

6. EGG OUTPUT: 240,000/♀/DAY; 7. MIGRATION: FROM BLOOD TO LUNG; 8. BORING HABIT: GOING DEEP INTO THE OPENINGS OF OTHER ORGANS ON THE INTESTINAL WALL

adults live for 1 year 240,000 eggs/ d

2. COMPLICATION OF ASCARIASIS 1. BILIARY ASCARIASIS: IS THE MOST COMMON COMPLICATION. 2. INTESTINAL OBSTRUCTION, 3. APPENDICITIS, 4. PERFORATION OF THE INTESTINE, 5. CHOLECYSTITIS, PANCREATITIS AND PERITONITIS

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Parasitology Exam Review 2015 3. PLEASE DESCRIBE THE LIFE CYCLE OF ASCARIS, AND PRESENT BRIEFLY THE CLINICAL MANIFESTATIONS OF ASCARIASIS. 1. LARVAE STAGE: MECHANISM: THE BLOOD-LUNG MIGRATION PHASE OF THE LARVAE: DURING THE MIGRATION THROUGH THE LUNGS, THE LARVAE MAY CAUSE A PNEUMONIA. >SYMPTOMS: ASCARIS PNEUMONITIS >LARGE NUMBERS OF WORMS MAY GIVE RISE TO ALLERGIC SYMPTOMS. >LOW FEVER, COUGH, BLOOD-TINGED SPUTUM, ASTHMA. 2. THE INTESTINAL PHASE OF THE ADULTS. 1)ASYMPTOM: A FEW ADULT WORMS USUALLY PRODUCES NO SYMPTOMS, BUT MAY GIVE RISE TO VAGUE ABDOMINAL PAINS OR INTERMITTENT COLIC, ESPECIALLY IN CHILDREN. 2) MALNUTRITION :A HEAVY WORM BURDEN CAN RESULT IN. 3) COMPLICATIONS OF ASCARIASIS: WANDERING ADULTS MAY BLOCK THE APPENDICLE LUMEN OR THE COMMON BILE DUCT AND EVEN PERFORATE THE INTESTINAL WALL. 4.DIAGONISTIC METHODS THE SYMPTOMS AND SIGNS ARE FOR REFERENCE ONLY. THE CONFIRMATIVE DIAGNOSIS DEPENDS ON THE RECOVERY AND IDENTIFICATION OF THE WORM OR ITS EGG. 1. ASCARIS PNEUMONITIS: EXAMINATION OF SPUTUM FOR ASCARIS LARVAE 2. INTESTINAL ASCARIASIS: FECES EXAMINATION FOR THE ASCARIS EGGS. (1) DIRECT FECAL FILM: IT IS SIMPLE AND EFFECTIVE. THIS METHOD IS THE FIRST CHOICE. (2) BRINE-FLOATATION METHOD: (3) DISCOVERY OF ADULT WORMS: WHEN ADULTS OR ADOLESCENTS ARE FOUND IN FECES OR VOMIT THE DIAGNOSIS MAY BE DEFINED.

Section 3 Trichiura, REMEMBER THE DEFFERENCE BETWEEN WHIPWORM AND ASCARIS IN LIFE CYCLE: 1. IT IS NO LARVA MIGRATION IN LIFE CYCLE. 2. THE ADULT WORMS LIVE IN THE CECUM. 1. LIFE CYCLE FEATURES 1. SITE OF INHABITATION: CECUM 2. INFECTIVE STAGE: EMBRYONATED EGG 3. INFECTIVE MODE AND ROUTE: SWALLOWED BY THE MOUTH 4. WITHOUT INTERMEDIATE HOST AND RESERVOIR HOST 5. THE LIFE SPAN OF THE ADULT IS ABOUT 3-5YEARS. 1.DIFFERENCE BETWEEN WHIPWORM AND ASCARIS IN LIFE CYCLE ASCARIS SITE OF INHABITATION UPPER PART OF SMALL INTESTINE INFECTIVE STAGE EMBRYONATED EGGS INFECTIVE ROUTE AND MODE BY MOUTH INTERMEDIATE HOST AND -------------------RESERVOIR HOST LIFE SPAN 1 YEAR

TRICHIURIA CECUM EMBRYONATED EGGS SWALLOWED BY MOUTH ----------------------3-5 YEAR

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Parasitology Exam Review 2015

Section 4 Hookworms 1. LIFECYCLE OF HOOKWORM（LARVA MIGRATION） 2. MAIN DIFFERENCES BETWEEN TWO HOOKWORMS 3. CLINICAL MANIFESTATIONS (LARVA MIGRATION, ADULT LIVE IN INTESTINE) 4. THE BEST DIAGNOSES METHOD FOR HOOKWORM 1. DIFFERENCE BETWEEN ASCARIS AND HOOKWORM IN LIFE CYCLE.

SITE OF INHABITATION INFECTIVE STAGE INFECTIVE ROUTE AND MODE

ASCARIS UPPER PART OF SMALL INTESTINE EMBRYONATED EGGS

BY MOUTH

HOOKWORM SMALL INTESTINE

LARVA 3 OR FILARIFORM LARVA

BY SKIN MAINLY, BY MOUTH MUCOSA, BY PLACENTA,

BY EATING TRANSPORT HOST MEAT OR RAW VEGETABLE

INTERMEDIATE HOST AND RESERVOIR HOST LIFE SPAN

-------------------1 YEAR

SOLUTION FOR IMPORTANT REVIEW

1. LIFECYCLE OF HOOKWORM（LARVA MIGRATION） 1. FINAL HOST: HUMAN 2. INF. STAGE: LARVA 3 OR FILARIFORM LARVA 3. INF. ROUTE: BY SKIN MAINLY, BY MOUTH MUCOSA, BY PLACENTA, BY EATING TRANSPORT HOST MEAT OR RAW VEGETABLE. 4. FOOD: BLOOD AND TISSUE FLUID 5. SITE OF INHABITATION: SMALL INTESTINE 6. LIFE SPAN: A.DUODENALE 2-15 YEARS, N. AMERICANUS 3-7YEARS 7. BLOOD-LUNG MIGRATION: SKIN→BLOOD CIRCULATION →RIGHT HEART→LUNG→TRACHEA→PHARYNX→SMALL INTESTINE 8. TRANSPORT HOST: PIG, MONKEY

-------------------A.DUODENALE 2-15 YEARS, N. AMERICANUS 3-7YEARS

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Parasitology Exam Review 2015 2. MAIN DIFFERENCES BETWEEN TWO HOOKWORMS

Shape

A.duodenale Adult are single curve, looks like C

Mouth capsule

the presence of 2 pairs of cutting "teeth," two on each side

Copulatory spicule

1pair with separate

Copulatory bursa

Circle in shape

N.americanus Adult are double curves, looks like S

the presence of two cutting “ plates”

unite to form terminal hooklet

Oval in shape

3. CLINICAL MANIFESTATIONS (LARVA MIGRATION, ADULT LIVE IN INTESTINE)

1. LARVAL STAGE (1) DERMATITIS, KNOWN AS "GROUND ITCH" OR "STOOL POISON". PAPULE WITH ITCHING. SCRATCHING LEADS TO SECONDARY INFECTION. (2)PNEUMONITIS: COUGH, ASTHMA, LOW FEVER, BLOOD-TINGED SPUTUM OR HEMOPTYSIS, CHEST-PAIN, INFLAMMATION， SHADOWS IN LUNGS UNDER X-RAY. THESE MANIFESTATIONS WENT ON ABOUT 2 WEEKS. 2. ADULTS IN SMALL INTESTINE (1) EPIGASTRIC PAIN : DUODENAL ULCER, GASTROINTESTINAL BLEEDING. (2) *MICROCYTIC HYPOCHROMIC ANEMIA: LASSITUDE, EDEMA, PALPITATION OF THE HEART. IN SEVERE CASE, DEATH MAY RESULT FROM CARDIAC FAILURE OR PHYSICAL EXHAUSTION. HEMOGLOBIN DECREASE (3) ALLOTRIOPHAGY: THE PATIENT WILL FELL COMFORTABLE, IF EAT SOIL, SAND, WOOL, PLASTIC BAGS, CLOTH. (4) INFANTILE HOOKWORM DISEASE: SEVERE SYMPTOMS THAN THE ADULT. DUODENAL ULCER, GASTROINTESTINAL BLEEDING, FECES WITH BLACK BLOOD, ANEMIA. (5) OTHERS: IN SERIOUS, CAUSING AMENORRHEA, STERILITY OR ABORTION FOR WOMEN.

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4. THE BEST DIAGNOSES METHOD FOR HOOKWORM definite diagnosis: find hookworm egg.

Method: 1. saturated brine flotation technique: this is the best choice mechanism: specific gravity of saturated brine is high than that of hookworm egg.

2. culture of larvae: eggs in the water →larvae. needs 5-7days.

3. check larvae from sputum 5. TREATMENT Drug for adult: ALBENDAZOLE, MEBENDAZOLE Treatment of anemia and malnutrition: Complement iron agent, blood transfusion, diet: rich in vitamin and protein。 Dermatitis of hookworm larvae: 15% THIABENDAZOLE OINTMENT 6. FUNCTION OF GLANDS ★ A pair of cephalic glands secrete the anticoagulant and acetylcholine esterase. ★3 pharyngeal glands open into the buccal cavity and pharyngeal cavity, and secrete acetylcholine esterase and proteinases. ★ anticoagulant: acting to prevent coagulation of blood ★ acetylcholine esterase: to destroy acetylcholine, impact transferring function of the neural medium, reduce wriggle of the worm.

7. PATHOGENISIS OF HOOKWORM ANEMIA 1.ABSORB BLOOD BY BUCCAL CAPSULE. 2.LIVE ON HOST BLOOD 3.RESISTANCE TO BLOOD CLOTTING BY SECRETING ANTICOAGULANT AND PROTEINASES 4. LEAVING BLEEDING POINTS, AND MIGRATE TO DIFFERENT ATTACHMENT SITE 5.THE DAMAGE OF MIGRATION 6. MALNUTRITION AND A LACK OF IRON. (OR) THE PATHOGENESIS OF HOOKWORM ANEMIA IS AS FOLLOWING: THE ANEMIA RESULTS FROM HOOKWORMS SUCKING BLOOD AND EXCESSIVE BLOOD LOSS. THE EXCESSIVE BLOOD LOSS IS DUE TO THE LARGE WORM BURDEN; WORMS SECRETING SEVERAL ANTIAGGLUTINATING MATERIALS (ANTIAGGLUTININ , AND ETC.), OFTEN CHANGING THE PLACE TO SUCK BLOOD AND DISCHARGING UNDIGESTED BLOOD; THE OLD INJURED SITES OF THE INTESTINAL WALL CONTINUING TO BLEED. THE OTHER REASON FOR THE ANEMIA IS THAT THE PATIENT CAN NOT GET ENOUGH NUTRITION. QUESTION FROM SENIORS 1. What’s the serious disease caused by hookworm? And what’s the mechanism?

Ans:- Adult hookworms cause “microcytic hypochromatic anemia”.

Each adult A. duodenale extracts 0.2ml of blood daily and N. americanus 0.03ml of blood.

The reason of anemia: 1) adults feed on the blood; 2) the wound blood can’t coagulate 3) change the site 4) the movement of the adults > The symptoms are lassitude, edema, palpitation of the heart. In severe case, death may result from cardiac failure or physical exhaustion. > Anemia can further lead to cause Atrophic glossitis, koilonychias,

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Section 5 Enterobius (pin worm) PPT REVIEW QUESTIONS 1. LIFE CYCLE (ESPECIALLY SITE OF OVIPOSITION: PERIANAL SKIN); 2. INJURE TO HUMAN. 3. WHAT IS THE RELATIONSHIP BETWEEN DIAGNOSES AND DISCHARGING EGGS FOR PINWORM？ > FEATURES OF LIFE CYCLE 1. SITE OF INHABITATION: CECUM(BLIND GUT) AND COLON(LARGE INTESTINE) 2. INFECTIVE STAGE: EMBRYONATED EGG(2RD STAGE) 3. INFECTIVE ROUTE: BY MOUTH 4. WITHOUT INTERMEDIATE HOST AND RESERVOIR HOST 5. LIFE SPAN OF FEMALE ADULTS: ABOUT 1 MONTHS 6. SITE OF OVIPOSITION: PERIANAL SKIN. > INJURE TO HUMAN (Symptomatology of Enterobiasis) 1. asymptomatic: About one-third of pinworm-infected persons are asymptomatic, The adult worms may cause slight irritation of the intestinal mucosa.

2. anal pruritus (perianal pruritus): The results is restless, nervousness, and irritability.  pruritus: which associates with the nocturnal migration of the gravid females around the anus and deposition of eggs in the perianal folds of the skin. which may lead to excoriations脱落 and bacterial superinfection.  Ectopic injure: adults can migrate into vagina, urethra, salpinx (oviduct) after lay eggs.

In women, migration of the worms may produce vaginitis阴道炎, peritonitis or granuloma of abdominal cavity, salpingitis causing sterility. moreover, invasion of the female to genital tract can cause vulvo-vaginitis and pelvic granulomas. > WHAT IS THE RELATIONSHIP BETWEEN DIAGNOSES AND DISCHARGING EGGS FOR PINWORM？ **** note this answer needed to be ensured Diagnosis 1. cellophane tape method：TO DISCOVERY OF THE CHARACTERISTIC EGGS. (THIS EXAMINATION SHOULD BE MADE IN THE MORNING, BEFORE THE PATIENT’S ANUS HAS WASHED OR DEFECATED ) 2. Adult worms are also diagnostic, to find it in the perianal area at night.

3. to find eggs occasionally in the stool, urine or vaginal secretion smears. >MCQ 1. Which of the following protozoa is known only in the trophozoite state?

A. Entamoeba histolytica B. Giardia lamblia C. Toxoplasma gondii D.Trichomonas vaginalis E. Leishmania Donovani ANS:: 2. A stool examination is the best method for diagnosing all but which of the following parasites?

A. Entamoeba histolytica B. Trichomonas vaginalis C. Cryptosporidium D. Giadia lamblia E. Ascaris lumbricoides ANS::

Section 6 Filaria 1、LIFE CYCLE OF FILARIA (INTERMEDIATE HOST) 2、FILARIASIS: ① MICROFILAREMIA;

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Parasitology Exam Review 2015 ② ACUTE MANIFESTATION PHASE: LYMPHANGITIS, LYMPHADENITIS, ETC. ③ CHRONIC OBSTRUCTIVE PHASE: ELEPHANTIASIS, CHYLURIA, HYDROCELE ④. SUPPRESSIVE FILARIASIS (TROPICAL EOSINOPHILIA SYNDROME) > FEATURES OF LIFE CYCLE 1.BIONEMATODE: INTERMEDIATE HOST IS MOSQUITOES; 2. INFECTIVE STAGE: FILARIFORM LARVA(L3); 3. INFECTIVE ROUTE: BY SKIN( THE WOUND BITTEN BY MOSQUITO ); 4. SITE OF INHABITATION: LYMPHATIC TISSUE; 5. LIFE SPAN: 10~15 YEARS; 6. MICROFILARIAE MAY SURVIVE 1-3 MONTHS; 7. VIVIPAROUS: ADULT LAY MICROFILARIA DIRECTLY 8. CONCEPT: NOCTURNAL PERIODICITY OF MICROFILARIAE 9. RESERVOIR HOST: CAT, MONKEY MAY BE THE RESERVOIR HOST OF B. MALAYI. HOWEVER, W. BANCROFTI HAS NO RESERVOIR HOST. 1. LIFE CYCLE OF FILARIA INTERMEDIATE HOST : MOSQUITO 1. DEVELOPMENT IN MOSQUITO MICROFILARIA

2.DEVELOPMENT IN HUMAN BODY FILARIFORM LARVA (L3)

FILARIFORM LARVA

ADULT

LAY MICROFILARIA

>WHAT IS THE MORPHOLOGICAL DIFFERENCES OF MICROFILARIA BETWEEN W. BANCROTI AND B. MALAYI? W. BANCROTI B. MALAYI APPEARANCE GRACEFUL, SWEEPING CURVES IRREGULAR, STIFF CURVES SIZE LARGER 244-296× 7 µM SMALLER 177-230 × 6 µM CEPHALIC SPACE SHORTER(1:1 OR1:2) LONGER(2:1) (LENGTH:WIDTH) NUCLEI BODY NUCLEI EQUAL SIZED, CLEARLY DEFINED, UNEQUAL SIZED, COALESCING, TERMINAL NUCLEI

COUNTABLE

UNCOUNTABLE

NO

TWO

>Microfilaremia :: (carrier) fever, lymphangitis there are many microfilaria in blood circulation. This symptom can persist for morn than 10 years. > Acute manifestation phase: This phase is actually an allergic response to SEA from eggs or the products of adolescent worms, or allergic response

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Parasitology Exam Review 2015 to the products of dying and degenerating adult worms. serum IgE level is elevated. > lymphangitis red swelling skin occur in lower or upper limb. the inflammation spreads centrifugally down the lymphatic channels of the leg Lymphadenitis: >Chronic obstructive phase Repeated attacks of acute lymphatic inflammations result in a chronic lymphedema with much fibrous infiltration, and consequently lymphatic obstruction. The lymph liquid return is obstructed and the lymph liquid “piles up”, greatly dilating, duct rupture, forcing the lymph into the surrounding tissues, causing diseases. >Elephantiasis: Skin becomes thicker, dry. some show lichen-like change, or verrucose growth. may occur in the limbs, scrotum, breast, vulva labium, etc. Elephantiasis legs are easily infected with bacteria or fungi >Chyluria (lymph in the urine) pre-aortic lymph nodes and intestinal lymphatic ducts anterior to chylocystis are obstructed. only caused by W. bancrofti. The chyle gives the urine a milky appearance. >Hydrocele: is caused by obstruction of lymphatics in testis and spermatic cord. only found in infection of Bancrofti. >Suppressive filariasis (Tropical eosinophilia syndrome: Is typeⅠ allergic reaction. cough, asthma, IgE level is elevated, eosinophilia.

>PATHOGENESIS AND MANIFESTATION OF LYMPHATIC FILARIASIS 1 MICROFILAREMIA (CARRIER) FEVER, LYMPHANGITIS. MICROFILAREMIA : THERE ARE MANY MICROFILARIA IN BLOOD CIRCULATION. THIS SYMPTOM CAN PERSIST FOR MORN THAN 10 YEARS 2. ACUTE PHASE: MECHANISM：LARVAE AND ADULTS LIVE IN THE LYMPH NODES AND LYMPHATIC VESSELS. METABOLITE OR SECRETION OF WORM EVOKE THE INFLAMMATORY RESPONSE. 3. CHRONIC OBSTRUCTIVE PHASE: MECHANISM:

(1) ELEPHANTIASIS: SKIN BECOMES THICKER, DRY, JUST LIKES ELEPHANT'S LEG. IT MAY OCCUR IN THE LIMBS, SCROTUM, BREAST, VULVA LABIUM, ETC. ELEPHANTIASIS LEGS ARE EASILY INFECTED WITH BACTERIA OR FUNGI. (2) CHYLURIA (LYMPH IN THE URINE) :: LYMPH-VESSEL OF RENAL PELVIS RUPTURED. ONLY CAUSED BY W. BANCROFTI. MANIFESTATIONS: THE CHYLE ENTER INTO URINARY SYSTEM, AND GIVES THE URINE A MILKY APPEARANCE. (3) HYDROCELE: HYDROCELE IS CAUSED BY OBSTRUCTION OF LYMPHATICS IN TESTIS OR SPERMATIC CORD. ONLY FOUND IN INFECTION OF BANCROFTI. MANIFESTATIONS: PATIENT’S SCROTUM ENLARGED, BUT THE SKIN IS THIN AND SMOOTH. MICROFILARIAE CAN BE FOUND IN HYDROCELE FLUID.

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Parasitology Exam Review 2015

(4) SUPPRESSIVE FILARIASIS (TROPICAL EOSINOPHILIA SYNDROME) MECHANISM: TYPEⅠALLERGY, IGE MANIFESTATIONS: COUGH, ASTHMA, IGE LEVEL IS ELEVATED, EOSINOPHILIA >NOCTURAL PERIODICITY OF MICROFILARIA. THE

MICROFILARIAE

CONCENTRATED

IN

THE

ARE SMALL

BLOOD VESSELS OF THE LUNG DURING THE DAY， AND ARE LIBERATED INTO THE PERIPHERAL BLOOD CIRCULATION AT NIGHT.

REVIEW QUESTIONS FOR NEMATODE 1. WHAT ARE THE DIFFERENCES OF LIFE CYCLE AND CLINICAL MANIFESTATIONS BETWEEN THE ASCARIS AND HOOKWORM? 2. WHAT IS THE PATHOGENESIS OF HOOKWORM ANEMIA? 3. WHAT ARE THE COMPLICATIONS OF ASCARIASIS? 4. WHAT ARE THE MAIN CLINICAL MANIFESTATIONS OF ASCARIS (HOOKWORM, FILARIA)?

5. WHAT’S THE BEST DIAGNOSES METHOD FOR ASCARIS (HOOKWORM, FILARIA, PINWORM)?

6. WHAT IS THE NOCTURNAL PERIODICITY OF MICROFILARIA? 7. WHAT IS THE MORPHOLOGICAL DIFFERENCES OF MICROFILARIA BETWEEN W. BANCROTI AND B. MALAYI?

Chapter 52 ARTHROPODA Introduction of Arthropoda 1.

2.

3.

4.

THE IMPAIRMENT OF ARTHOPODS TO HUMAN (INDIRECT IMPAIRMENT) TWO METHODS FOR ARTHROPODS TRANSFERRING THE PATHOGEN METHODS FOR CONTROL OF MEDICAL ARTHROPODS (SIX ASPECTS) SOME TERMS

SOLUTION FOR IMPORTANT REVIEW 1.

THE IMPAIRMENT OF ARTHOPODS TO HUMAN ARE :: 1．DIRECT IMPAIRMENT (DIRECT INJURY) :: ANNOYANCE AND SUCKING BLOOD POISON LESION [ TICK PARALYSIS IS CAUSED BY SALIVARY VENOM OF SOME HARD TICKS. VENOM OF SCORPION AND SPIDER MAY EVEN CAUSE DEATH.]

ALLERGIC REACTION [ BEE AND WASP STING CAN CAUSE DEATH, DUST MITES CAUSE ASTHMA OR ALLERGIC RHINITIS, SOME PEOPLE ARE ALLERGIC TO

DIRECT PARASITES [ ITCH MITE

COCKROACH PROTEINS.]

INFESTATION CAUSE HUMAN SCABIES, FOLLICLE MITE CAUSE DEMODICIDOSIS, MYIASIS IS CAUSE BY FLY LARVAE (MAGGOT)]

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Parasitology Exam Review 2015 2．INDIRECT IMPAIRMENT (VECTORS FOR PATHOGENS INCLUDING MICROORGANISMS, VIRUSES AND PARASITES) VECTOR BORN DISEASES: THE DESEASES TRANSMITTED BY ARTHROPOD VECTORS.

INDIRECT IMPAIRMENT IS THE MOST IMPORTANT HARM WAY OF ARTHROPODS TO HUMAN HEALTH. (1) MECHANICAL TRANSMISSION :: THE ARTHROPODS PLAY THE ROLE ONLY IN TRANSFERRING THE PATHOGENS AS PASSIVE CARRIER. IN THE PROCESS THE MORPHOLOGY AND NUMBERS OF PATHOGENS DO NOT CHANGE. (2) BIOLOGICAL TRANSMISSION :: THE ARTHROPODS ARE USED BY DISEASE-PRODUCING ORGANISMS NOT ONLY AS A VEHICLE BUT ALSO AS AN ENVIRONMENT FOR DEVELOPMENT. 2. MECHANICAL & BIOLOGICAL TRANSMISSION 3. METHODS FOR CONTROL OF MEDICAL ARTHROPODS (SIX ASPECTS)      

1.ENVIRONMENT MANAGEMENT: CLEAN ENVIRONMENT 2.PHYSICAL CONTROL: SCREEN, SUNSHINE 3.CHEMICAL CONTROL: INSECTICIDE 4.BIOLOGICAL CONTROL [BACILLUS THURINGIENISIS CAN PARASITE IN MOSQUITO LARVAE. FISH CAN EAT MOSQUITO LARVAE IN POOL.] 5.GENETIC CONTROL 6.THE METHODS BY LAWS

4.TERMS (SEE REVIEW QUESTIONS) 1. MOLT :: MOLTING IS THE SHEDDING OF OLD CUTICLE AND EXPANDING INTO A NEW AND LARGER ONE QUESTIONS FOR REVIEW

1. WHAT IS THE MEDICAL ARTHROPODOLOGY? MEDICAL ARTHROPODOLOGY IS A BIOLOGICAL SCIENCE, WHICH RESEARCHES ARTHROPODA MORPHOLOGY, LIFE CYCLE, ECOLOGY, THE DAMAGE TO HUMAN OR ANIMALS AND PREVENTION MEASURES FOR ARTHROPOD INJURY. THE INSECTA IS THE MOST IMPORTANT CLASS WITH THE MOST SPECIES AND THE LARGEST NUMBERS. MEDICAL ENTOMOLOGY IS ALSO CALLED MEDICAL ARTHROPODA. 2. WHAT IS THE MOST IMPORTANT MEDICAL ARTHROPODS? MEDICAL ARTHROPODOLOGY IS CLASSIFIED INTO 5 CLASSES : 1) INSECTA: THE MOST IMPORTANT 2) ARACHNIDA: 2ND IMPORTANT 3) CRUSTACEA 4) CHILOPODA: SCOLOPENDRA 5) DIPLOPODA: MILLIPEDE

AMONG THESE CLASS INSECTA IS THE IMPORTANT ONE. 3. CONCEPTS: • INDIRECT IMPAIRMENT OF ARTHROPODA? INDIRECT IMPAIRMENT (VECTORS FOR PATHOGENS INCLUDING MICROORGANISMS, VIRUSES AND PARASITES) :: TRANSFERRING THE PATHOGENS . VECTOR BORN DISEASES: THE DESEASES TRANSMITTED BY ARTHROPOD VECTORS. INDIRECT IMPAIRMENT IS THE MOST IMPORTANT HARM WAY OF ARTHROPODS TO HUMAN HEALTH. MECHANICAL TRANSMISSION? MECHANICAL TRANSMISSION :: THE ARTHROPODS PLAY THE ROLE ONLY IN TRANSFERRING THE PATHOGENS AS PASSIVE CARRIER. IN THE PROCESS THE MORPHOLOGY AND NUMBERS OF PATHOGENS DO NOT CHANGE. • BIOLOGICAL TRANSMISSION? BIOLOGICAL TRANSMISSION :: THE ARTHROPODS ARE USED BY DISEASE-PRODUCING ORGANISMS NOT ONLY AS A VEHICLE BUT ALSO AS AN ENVIRONMENT FOR DEVELOPMENT. • METAMORPHOSIS? WHEN HATCHED FROM EGGS, INSECTS UNDERGO A SERIES OF MORPHOLOGICAL, BEHAVIORAL AND ECOLOGICAL CHANGES UNTIL THEY BECOME SEXUALLY MATURED ADULTS, AND THIS PROCESS IS CALLED METAMORPHOSIS. THERE ARE TWO TYPES OF METAMORPHOSIS ::

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Parasitology Exam Review 2015 1) INCOMPLETE METAMORPHOSIS

2) COMPLETE METAMORPHOSIS

INCOMPLETE METAMORPHOSIS

COMPLETE METAMORPHOSIS

COMPARE TO ADULTS THE NYMPHS FEATURES:

⑴ NYMPH IS SMALLER; ⑵ NYMPH IS IMMATURE

• INCOMPLETE METAMORPHOSIS? INSECTS WITH INCOMPLETE METAMORPHOSIS UNDERGO THREE BASIC STAGES (EGG, NYMPH, ADULT) AND THE NYMPH IS SIMILAR TO ADULT MORPHOLOGICALLY. • COMPLETE METAMORPHOSIS? INSECTS WITH COMPLETE METAMORPHOSIS UNDERGO FOUR BASIC STAGES (EGGS, LARVAE, PUPAE AND ADULTS) IN THEIR LIFE CYCLE AND THEIR LARVAE BEAR LITTLE RESEMBLANCE TO THE ADULTS. 5. WHAT KINDS OF DISEASES DO MOSQUITOES TRANSMIT TO HUMAN? MALARIA 6. WHAT CLASS DO MOSQUITOES OR FLIES BELONG TO? CLASS INSECTA 7. WHAT CLASS DO TICKS AND MITES BELONG TO?

CLASS ARACHNIDA PREVIOUS YEAR REVIEW QUESTION CLASS INSECTA

CLASS ARACHNIDA

1.3 body segments- head, thorax (chest), abdomen (stomach area).

2.three pairs of legs 3. 1 pair of antennae 4.some species have one or two pairs of wings Representative group： mosquito, fleas, flies The insects are the most numerous and diverse of all the groups of arthropods.

1.☆No antennae and wings 2.☆the body has two regions: cephalo thorax and abdomen or is fused together into one part.

3.☆ four pairs of jointed legs Representative group： Ticks, mites, and spiders.

REVIEW QUESTIONS FOR ARTHROPODS 1. WHAT IS THE MEDICAL ARTHROPODOLOGY? 2. WHAT IS THE MOST IMPORTANT MEDICAL ARTHROPODS? 3. HOW MANY CLASSES DO THE ARTHROPODS INCLUDE? 4. MOLT? METAMORPHOSIS? COMPLETE METAMORPHOSIS? INCOMPLETE METAMORPHOSIS? 5. WHAT KINDS OF DISEASES DO MOSQUITOES TRANSMIT TO HUMAN? 6. WHAT CLASS DO MOSQUITOES OR FLIES BELONG TO? 7.WHAT CLASS DO TICKS AND MITES BELONG TO?

TERMS PARATENIC HOST (TRANSPORT HOST): IS AN ABNORMAL HOST IN WHICH SOME PARASITIC LARVAE CAN SURVIVE BUT CAN’T DEVELOP INTO THE ADULT STAGE. IF THE LARVAE HAVE A CHANCE TO ENTER THEIR APPROPRIATE HOSTS, THEY CAN CONTINUE TO DEVELOP INTO ADULTS THERE

CONCOMITANT IMMUNITY : THIS IS AN INCOMPLETE IMMUNITY OR NON-STERILIZING IMMUNITY. IT CAN RESIST TO LARVAE REINFECTION, BUT CAN NOT ELIMINATE THE ADULT SCHISTOSOMES FROM THE HOST. THE RESISTANCE WILL DISAPPEAR AS SOON AS LIVING SCHISTOSOMES ARE COMPLETELY ELIMINATED BY DRUG.

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Parasitology Exam Review 2015

CARRIER : A PERSON WHO HARBOURS PARASITE HAS NO CLINICAL SYMPTOMS, IS AN IMPORTANT SOURCE OF INFECTION IN EPIDEMIOLOGY.THE PARASITE CAN BE DETECTED BY NORMAL EXAMINATION. CYSTICERCOSIS : THE LARVAL STAGE (CYSTICERCUS CELLULOSE) LIVES IN PIG OR HUMAN TISSUES CAUSING CYSTICERCOSIS INCOMPLETE METAMORPHOSIS : INSECTS WITH INCOMPLETE METAMORPHOSIS UNDERGO THREE BASIC STAGES (EGG, NYMPH, ADULT) AND THE NYMPH IS SIMILAR TO ADULT MORPHOLOGICALLY NOCTURAL PERIODICITY OF MICROFILARIAE :: A CIRCADIAN RHYTHM WITH THE PERIODICITY EXPRESSED DURING NIGHTTIME HOURS, AS IN THE NIGHT RELEASE OF MICROFILARIAE OF THE HUMAN FILARIA WUCHERERIA BANCROFTI INTO THE PERIPHERAL BLOOD.THE MICROFILARIAE ARE CONCENTRATED IN THE SMALL BLOOD VESSELS OF THE LUNGS DURING THE DAY AND ARE LIBERATED INTO THE PERIPHERAL BLOOD CIRCULATION AT NIGHT. CERCARIAL DERMATITIS : WHEN SCHISTOSOME CERCARIA REPEATEDLY PENETRATE THE HUMAN SKIN, ALLERGY I AND IV TAKES PLACE. THE CERCARIAL DERMATITIS APPEARS: ITCH, LOCAL EDEMA, RASHES(PAPULES, ERYTHEMA), A FEW HOURS AFTER CONTACTING INFESTED WATER, LASTING ABOUT 2-3DAYS.

DERMATITIS OF HOOKWORM LARVA: KNOWN AS "GROUND ITCH" OR "STOOL POISON". PAPULE WITH ITCHING. SCRATCHING LEADS TO SECONDARY INFECTION. PNEUMONITIS OF HOOKWORM LARVA : COUGH, ASTHMA, LOW FEVER, BLOOD-TINGED SPUTUM OR HEMOPTYSIS, CHESTPAIN, INFLAMMATION， SHADOWS IN LUNGS UNDER X-RAY. THESE MANIFESTATIONS WENT ON ABOUT 2 WEEKS. MECHANICAL TRANSMISSION : THE ARTHROPODS PLAY THE ROLE ONLY IN TRANSFERRING THE PATHOGENS AS PASSIVE CARRIER. IN THE PROCESS THE MORPHOLOGY AND NUMBERS OF PATHOGENS DO NOT CHANGE. BIOLOGICAL TRANSMISSION :: THE ARTHROPODS ARE USED BY DISEASE-PRODUCING ORGANISMS NOT ONLY AS A VEHICLE BUT ALSO AS AN ENVIRONMENT FOR DEVELOPMENT. PARASITISM: IS THE ASSOCIATION OF TWO DIFFERENT ORGANISMS, IN WHICH ONE PARTNER IS BENEFITED WHILE THE OTHER IS INJURED, SUCH AS ASCARIS LUMBRICOIDES AND HUMAN. TWO PARTNERS OF PARASITISM ARE :: PARASITE, HOST INFECTIVE STAGE: IS A STAGE WHEN A PARASITE CAN INVADE HUMAN BODY AND LIVE IN IT.

OPPORTUNISTIC PARASITE: THE PARASITE IN AN IMMUNOCOMPETENT HOST IS LOW VIRULENCE THAN SELDOM PRODUCES DISEASE AND CAN’T BE DETECTED BY NORMAL EXAMINATION BUT INFECTION IN AN IMMUNOCOMPROMISED (SUCH AS AIDS) HOST MAY BE MANIFESTED BY SEVERE DISEASE, SOMETIMES BE LETHAL

CHRONIC INFECTION:

SUPPRESSIVE INFECTION:

LARVA MIGRANS:

MEANS THAT WHEN LARVA LIVE IN THEIR ABNORMAL HOST, THEY CANNOT GROW INTO ADULTS BUT CAN

WANDER EVERYWHERE AND CAUSE THE LOCAL OR SYSTEMIC PATHOLOGICAL LESION OF THE HOST. SUCH AS A LARVAL STAGE OF ASCARIS CANIS IN OUR BODY.

ECTOPIC PARASITISM:

NON STERILIZING IMMUNITY: THE IMMUNITY CAN’T CLEAN UP THE PARASITES IN THE HOST, BUT MAY PROTECT THE BODY FROM SUPERINFECTION AS LONG AS THE PARASITES REMAIN IN THE BODY. THIS MAY BE OF GREAT IMPORTANCE IN ENDEMIC AREAS IN LIMITING THE SEVERITY OF INFECTION WITH PLASMODIUM, SCHISTOSOME, HOOKWORMS AND OTHER PARASITES. From Review terms by Ma’am • FINAL OR DEFINITIVE HOST---- the host in which sexual reproduction of parasites occurs or the host parasitized by adult worm is called ~ • INTERMEDIATE HOST-----------the species in which larval stage or asexual reproduction of the parasite occurs is called ~ • RESERVOIR HOST-------------- a vertebrate is parasitized by the same stage of same parasites as that done in human and serves as the infective source of human infection, which is called~

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Parasitology Exam Review 2015

• PARATENIC HOST-------------- when some helminthic larvae invade into a un-adapatable host, they can’t grow but survive. If the host is eaten by definitive host, the larvae finally become adult worms. This unsuitable host is called paratenic or transport host.

• RECRUDESCENCE: reattacks occur again following a period of weeks or months without any symptoms, but with lower-grade of parasitemia.The reason is that there are few parasites remain in RBC,and reproduce in some condition.

• RELAPSE : reattacks occur again following a period of weeks or months without any symptoms。It’s result from reactivating of hypnozoite forms of the parasite in the liver cells.

FILL IN THE BLANKS 1.Occasionally, the adults of Spirometra mansoni are parasitic in the _______ of human, but it hardly causes a clinical problem. In contrast, human parasitism with the larva, ________, may sometimes be fatal.

Ans::

2.S.japonicum inhabitate in ________ of humans. The water containing ________ is called infested water. Pathogenesis of S.japonicum is almost entirely due to the stage of _________.

Ans::

FEW QUESTIONS FROM SENIORS 1.What protozoa can cause diarrhea? And what’s the mechanism?

Ans:Entamoeba histolytica:In Acute Intestinal Amoebiasis the patients show symptoms of diarrhea or dysentery.

Mechanism: 1. Adherence of trophozoites on the surface of the large intestine; 2. Invasion of the large intestine; (trophozoits can secrete numerous proteolytic enzymes, et al) 3. Resistance of the amoebae to various effector mechanisms of the host.

Trophozoites may penetrate the muscular coats and occasionally the serosa, leading to perforation into the peritoneal cavity peritonitis Cryptosporidium parvum It can cause Cryptosporidiosis which resulting in diarrhea and the most severe infections in immunecompromised individuals Mechanism: The adhesion invasion of C.parvum sporozoites or merozoites to the apical membrane of intestinal epithelial cells stimulate the activity of several cellular kinases that participate in the cytoskeletal rearrangement associated with C.parvum invasion of the cell.  Cellular invasion stimulate intestinal secretion in response to cellular infection and results in flattened and fused small intestinal villi Giardia Lamblia diarrhea is typical.the stool is foul smelling, greasy in appearance, floats on water and without blood or mucus. Upper abdominal cramping, abdominal distention, sulfuric, eructatio flatus.

Pathogenic mechanism G. lamblia is usually weakly pathogenic for humans.  Mechanical blockade of the intestinal mucosa by large numbers of Giardia  Affect the intestinal absorption of nourishment(crypt. hypertrophy, villous atrophy or flattening, epithelial cell damage)  Disaccharidase deficiency with lactose(fatty diarrhea )

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Parasitology Exam Review 2015

PREVIOUS YEAR QUESTION PAPER Theory examination of Parasitology of Human I. Choosing the best answer (1 point each; 30 points total). In a few cases, the A, B, C, D or E may be used more than once.

Item 16~19 16. Clinical Manifestations for ascariasis 17. Clinical Manifestations for Trichuriasis 18. Clinical Manifestations for hydatidosis 19. Clinical Manifestations for Sarcoptes scabiei A. abdominal pain and diarrhea B. perianal pruritus D. giant Liver and spleen

C. elephantiasis

E. scabies

Item 20~21 20. Clinical Manifestations for schistosomiasis 21. Clinical Manifestations for hydatidosis A. liver cirrhosis B. portal vein hypertension C. the both D. neither A nor B Item 22~24 22. The best drug useful for treating schistosomiasis 23. The best drug useful for treating Filariasis 24. The best drug useful for treating Taeniasis 25. The best drug useful for treating Trichuriasis A. Albendazole B. Praziquantel

C. Hetrazan (diethylcarbamazine, DEC)

D. Metronidazole E. Primaquine Item 26~29 26. The best diagnosis method for Intestinal ascariasis 27. The best diagnosis method for Hookworm 28. The best diagnosis method for Enterobiasis 29. The best diagnosis method for Filariasis A. Direct fecal film

B. fecal saturated brine flotation method

D. cellophane tape method

C. blood smear

E. Examination of sputum

30. Infective stage for Schistosoma japonicum A. Taenia egg B. csty C. metacercariae

D. Cysticercus E. cercariae

IIďź&#x17D;Filling following lined blank (1 point each; 20 points total) 1. People acquire infection of Clonorchis sinensis by eating with

.

or

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Parasitology Exam Review 2015

2. Paragonimus westermani mainly lives in or

(organ) of human, it can be diagnosed by examining

(specimen).

3. Wipeworm inhabitate in

of human.

4. The adult of lymphatic filaria inhabitate in lymphatic system of humans. B. malayi live in superficial lymphatic system. While, W. bancrofti live in

, besides in shallow lymphatic system.

Manifestations of lymphatic filariasis for chronic obstructive phase are

and so on.

III. Explaining the following concepts (3 points each; 18 points total): 1. bean-pork 2. Nocturnal periodicity of microfilariae 3. Ascaris pneumonitis 4. ground itch(stool poison ) 5. Cysticercosis 6. cercarial dermatitis

IV. Answer the following questions (8 point each; 32 points total) 1. Presentation the differences in Morphology and lesion to human between T. solium and T. saginata.

(8 points) 2. Diagram the complete life cycle of S. japonucum. The adults of S. japonucum inhabit in mesenteric vein and lay eggs in inferior portal vein systemďź&#x152; why are its eggs discharged with fecesďź&#x; (8 points) 3. How to diagnose Enterobius vermicularis? How to treat and prevent the Enterobiasis?

(8 points)

4. Compare the differences between hook worm and Ascaris in life cycle and symptom.

Theory test mode with answers I. Choosing the best answer (1 point for each question).

In a few cases, the A, B, C, D or E may be used more than once. But ,the answer is just one. For example: 1. Which of the following description about hydatid disease is wrong? (C) A. Canivores serve as final hosts.

B. Human is infected by the egg of Echinococcus granulosus.

C. Human hydatid disease is caused by adult worm.

D. Herbivores serve as intermediate hosts.

2~5 2. Clinical Manifestations for Enterobiasis (B) 3. Clinical Manifestations for Trichuriasis (A) 4. Clinical Manifestations for fasciolopsiasis (A) 5. Clinical Manifestations for Schistosoma japonicum (D) A. abdominal pain and diarrhea B. perianal pruritus C. elephantiasis D. giant Liver and spleen E. scabies Item 6~7

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Parasitology Exam Review 2015

6. Clinical Manifestations for schistosomiasis (C) 7. Clinical Manifestations for hydatidosis A. liver cirrhosis B. portal vein hypertension C. the both D. neither A nor B IIďź&#x17D;Filling following lined blank (1 point each) 1. People acquire infection of Clonorchis sinensis by eating Fish or Shrimp with Metacercaria.

2. Paragonimus westermani mainly lives in (organ) of human, it can be diagnosed by examining sputum or Stool (specimen).

3. Occasionally, the adults of Spirometra mansoni are parasitic in the Small intistine but it hardly causes a clinical problem. In contrast, sparganosis mansoni with the larva, plerocercoid, may sometimes be fatal.

of humans,

III. Explaining the following concepts (2 points each): 1. Parasitism - is the association of two different organisms, in which one partner is benefited(parasite) while the other is injured(host).

-Eg: ascaris lumbricoides(paarasite) and human(host) 2. infective stage - :- it is the stage in which the parasite invade the human body and live in it.

3. Cysticercosis - It is caused by cysticercus or larva of the pork tapeworm (taenia solium). The manifestations vary with the number of cysticerci in the tissues and organs of the body, such as the subcutaneous tissues, muscles, heart, lungs, liver, brain and eye. There are three types of cysticercosis: i) cysticercosis in subcutaneous tissue and muscle ( cysticercosis in tongue) ii) ocular cysticercosis iii) brain cysticercosis 4. pneumonitis of hookworm larva - Caused by the migration of hookworm larva.

- An allergic reaction:cough, asthma, low fever, blood-tinged sputum or hemoptysis, chest-pain, inflammationďź&#x152; shadows in lungs under X-ray.

- These manifestations went on about 2 weeks.

IV. Answer the following questions (8 point each) What is the Pathogenesis of hookworm anemia?

The Pathogenesis of hookworm anemia is as following: The anemia results from hookworms sucking blood and excessive blood loss. The excessive blood loss is due to the large worm burden; worms secreting several antiagglutinating materials (antiagglutinin , and etc.), often changing the place to suck blood and discharging undigested blood; the old injured sites of the intestinal wall continuing to bleed. The other reason for the anemia is that the patient can not get enough nutrition.

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