Human Parasitology
Section I INTRODUCTIONTO PARASITOLOGY
Parasitology（寄生蟲(chóng)學(xué)), the study of parasites（寄生蟲(chóng)) and their relationships to their hosts（宿主), is one of the most fascinatingareas of the biology. While it is entirely proper to classify many bacteria（細(xì)菌) and fungi（真菌) and all viruses as parasites,parasitology has traditionally been limited to parasitic protozoa（原蟲(chóng)), helminthes（蠕蟲(chóng)), and arthropods（節(jié)肢動(dòng)物), as well as those species ofarthropods that serve as vectors（媒介)for parasites. It follows, then, that parasitology encompasseselements of protozoology（原蟲(chóng)學(xué)), helminthology（蠕蟲(chóng)學(xué)), and medical arthropodology（醫(yī)學(xué)節(jié)肢動(dòng)物學(xué)).
Human parasitology, an important part ofparasitology, study the medical parasites including their morphology(形態(tài)學(xué)),
life cycle（生活史), the relationship with host and environment. The objectives are tostudy the way or the measurement of parasitic diseases control.
GENERAL CONSIDERATION
Medical (human) Parasitology consists ofmedical protozoology, medical helminthology, and medical arthropodology.
Symbiosis（共生)
Commensalism（共棲)
Mutualism（互利共生)
Parasitism（寄生) Parasite（寄生蟲(chóng))
Host
1) Definitive host（終宿主)
2) Intermediate host（中間終主)
3) Reservoir host（保蟲(chóng)宿主)
4) Paratenic host or transport host（轉(zhuǎn)續(xù)宿主)
TRANSMISSION OF PARASITES
Source of infection（傳染源)
1) Humans
2) Animal zoonoses人獸共患病
Mode of transmission（傳播方式)
1) Oral route
2) Penetration of the skin and mucousmembrane
3) Inoculation by an arthropod vector
4) Sexual contact
PARASITIC ZOONOSES(人獸共患病)
These are the infections which are naturallytransmitted between the vertebrate animals and man. The condition usuallyincludes those infections in which the proof of strong circumstantial evidenceof transmission between the man and animals are documented.
PATHOGENESIS AND PATHOLOGY（發(fā)病機(jī)制與病理學(xué))
Pathogenesis（發(fā)病機(jī)制)
TableⅠ-Ⅰ-2 PathogenicMechanisms in Parasitic Diseases
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Mechanism Parasitic diseases
Trauma Strongyloidiasis, enterobiasis, taeniasis,clonorchiasis,
schistosomiasis and hookworm infection
Invasion and destruction of host cell Malaria,leishmaniasis,trypanosomiasis,
toxoplasmosis and amoebiasis
Inflammation Trichnellosis, lymphatic filariasis, paragonimiasis,
Amoebiasis
Toxin Amoebiasis,Chaga’s disease and sleeping sickness
Allergic manifestation Schistosomiasis, hydatid disease
HOST IMMUNITY
IMMUNOEVASION OF PARASITES（寄生蟲(chóng)免疫逃避)
CLINICAL MANIFESTATION（臨床表現(xiàn))
Clinical manifestation of parasiticdiseases are variable. It may be acute or chronic. However, many of thediseases are chronic in nature. The onset of the disease is slow. In a fewparasitic diseases, the onset may be sudden. For example, in ascariasis,pneumonitis develop immediately few days after ingestion of Ascaris蛔蟲(chóng) eggs. Ingestion of pork infectedwith the larvae of Trichinella spiralis旋毛蟲(chóng), causes gastro-intestinal disturbances within a few hours,simulating food-poisoning.
Allergic manifestation are important inmany a helminthic infections. Schistosoma eggs produce an allergic reaction inthe host tissue. Similarly, the adult Brugia and Wuchereria worm in thelymphatics cause frequent attacks of filarial fever, lymphangitis, etc. Avariety of localized and generalized allergic and neurological manifestationsmay be caused by inoculation of toxins into the skin by arthropods, during thebite.
DIAGNOSIS
TREATMENT
PREVENTION AND CONTROL
PARASITOLOGY IN FUTURE
SectionⅡ PROTOZOA (原蟲(chóng))
Ⅰ.INTRODUCTION
Protozoa are usually defined as singlycelled animals, they belonging to the animal kingdom, subkingdom Protozoa.
MORPHOLOGY
Protozoa, that is, the whole body consistsof a singular cell. Like a cell in the tissue of metazoa, a protozoan cell iscomposed of plasma membrane (原生質(zhì)膜), cytoplasm (細(xì)胞質(zhì)) and nucleus.
Plasma membrane: The membrane appears three layered inelectron micrographs because the central lipid portion looks light or clear(electron lucent) and is enclosed by the darker (electron dense) protein layer.The trilaminar unit membrane support by a sheet of contractile fibrils, whichenable the cell to change its shape and help in locomotion protection &nutrition.
Cytoplasm: The cytoplasm matrix consists ofvery small granules and filaments suspended in al low-density medium withphysical properties of a colloid. In some species, the cytoplasm is divisibleinto two portions: ectoplasm (外質(zhì)) and endoplasm (內(nèi)質(zhì)).
1) ectoplasm: The ectoplasm is the outertransparent layer with function of protection, locomotion and sensation. It isoften in the gel state.
2) endoplasm: The endoplasm is the inner granularlayer containing vacuoles and organelles. It is in the sol state of thecolloid, and it bears the nucleus, mitochondria, Golgi bodies, and so on. Thesecan only be visualized by electron microscopy. The endoplasm helps in nutritionand reproduction.
3) Organelles(細(xì)胞器): There are several membraneorganelles characteristic of eukaryotes (真核細(xì)胞), such as endoplasmic reticulum, mitochondria, variousmembrane-bound vescles, and Golgi bodies, are usually found in protozoa.Mitochondria that bear the enzymes of oxidative phosphorylation and tricarboxylicacid cycle often have tubular rather than lamellar cristae in protozoa,althougher they may be absent.
Protozoa have several locomotory organelles(運(yùn)動(dòng)細(xì)胞器):flagella (鞭毛), cilia (纖毛), and pseudopodia (偽足). Flagella are long delicatethread like filaments; flagella composed a central axoneme and an out sheaththat is a continuation of the cell membrane. A flagellum is capable of avariety of movements, which may be fast or slow, forward, backward, lateral, orspiral. Pseudopodia are temporary organelles found in Sarciodina (肉足類(lèi)) (and other organisms) thatcause the organism to move and aid it in capturing food. They do not occur inall sarciodines. Cilla are structurally similar to flagella, they are fineneedle like filaments covering the entire surface of the body.
Some species of protozoa have rudimentarydigestive organs such as cytostome and cytopharynx.
Nuclei: it is the vital structure of acell. It is present in the endoplasm. A membrane known as nuclear membranesurrounds nucleus externally. In all protozoa excepting Balantidium coli, thenucleus is vesicular. Nucleus contains a karyosome (核仁) and chromatin granules.
Trophozoite(滋養(yǎng)體): It is the reproductive stageof the most protozoa (e.g., intestinal flagellate, amoebae, and ciliates). Itis active feeding stage of the parasite and this stage is associated with thepathogenesis of the disease.
Cyst(包囊): It is theresistant form of the protozoa with a protective membrane or thickened wall. Itis produced during unfavorable circumstances. The protective wall of cystenables the parasite to survive outside the host in an environment underadverse circumstance for a variable period ranging from a few days to years.
The cyst is resting stage ofthe parasite. Replication usually does not occur in this stage. However,multiplication may occur in the cysts of some species (e.g., Entamoeba histolytica),where the nucleus divides to produce asexually. The cysts formed sexually arecalled oocysts.
TYPE OF LIFE CYCLE
Person to Person transfer (人際傳播型)
Circulation transfer(循環(huán)傳播型)
Vector transfer（蟲(chóng)媒傳播型)
PATHOLOGIC CHARACTERISICS OF PROTOZOA
1) Multiplication (增殖): protozoa reproduce in theirhost, when the number is enough, they may destroy the infected cells, or theymay invade other tissue of host, and produce pathological change on host.
2) Opportunistic pathogen (機(jī)會(huì)致病) ：Some symbiotic protozoa are nonpathogenic or cause only limitedclinical symptoms in immunocompetent host, but produce serious symptoms inimmunodeficient persons.
CLASSIFICATION OF PROTOZOA
Ⅱ ENTAMOEBAHISTOLYTICA (溶組織內(nèi)阿米巴)
Entamoeba coli (結(jié)腸內(nèi)阿米巴),
Entamoeba dispar (迪斯帕內(nèi)阿米巴)
MORPHOLOGY
The parasite occurs in 3 stage:trophozoite, precyst and cyst.
Trophozoite(滋養(yǎng)體): (Fig1)
Cyst（包囊):
Fig Ⅱ－Ⅱ－2 Trophozoite and cyst of Entamoeba histolytica
LIFE CYCLE
Fig Ⅱ－Ⅱ－3 Life cycle of E. histolytica, Adapted from parasite image libraryof CDC, USA
The mature cysts (成熟包囊) excreted in the feces are theinfective forms. They unlike the trophozoites which degenerate within minutes,may remain viable for weeks or months in suitable moist environment. Cysts ofE. histolytica can remain viable and infective in a moist, cool environment forat least 12 days, and in water they can live up to 30 days. They are rapidlykilled by putrefaction, desiccation, and temperatures below -5℃and above 40℃. They canwithstand passage through the intestine of flies and cockroaches. The cysts areresistant to levels of chlorine normally used for water purification. Thesecysts cause infection in other susceptible persons through faecal contaminationof water and vegetables or direct faecal-oral contact and the cycle isrepeated.
PATHOGENESIS AND CLINICAL MENIFESATTIONS
Pathogenic mechanism: Amoebiasis (阿米巴病) is a disease caused bypotentially pathogenic strains of E. histolytica. These pathogenic amoebaecause invasive amoebiasis through the sequential stages of: a) Adherence oftrophozoites on the surface of the large intestine. b) Invasion of the largeintestine by the amoebae, and finally c) Resistance of the amoebae to varioureffector mechanisms of the host.
Symptoms
ⅠAsymptomaticinfections
ⅡSymptomaticinfections
A. Intestinal amebiasis: (1) Dysenteric; (2) Nondysenteric clitis
B. Extraintestinal amebiasis:
(1) Hepatic: a. Acute nonsuppurative;b.liver abscess
(2) Pulmonary
(3).Other extraintestinal foci (very rare)
E. histolytica infection in man isvariable. In endemic area, nearly 90% of individuals harbouring E. histolyticain their intestinal tract are asymptomatic cyst passers, while remainders haveinvasive intestinal amoebiasis or extra-intestinal invasive amoebiasis such asamoebic liver abscess.
Incubation period is usually long and often indefinite. It may be shortin rare instances.
1) Intestinal amoebiasis(腸阿米巴病): Intestinal amebiasis is themost common form of infection and may be asymptomatic (無(wú)癥狀的). Certain patients withintestinal amebiasis have vague and nonspecific abdominal symptoms. Acuteamoebiasis patients have more definite symptoms, such as diarrhea or dysentery (痢疾，腹瀉), abdominal pain and cramping,flatulence (腸胃氣漲),anorexia (食欲減退), weightloss, and chronic fatigue. This term should be reserved for those who actuallyhave dysentery.
①Asymptomaticcyst passers: It is the common clinical form of intestinal amoebiasis. Gastrointestinalmanifestations are not specific. It consists of colicky lower abdominal painand increased frequency of bowel movements with loose watery diarrhoea. Thecondition is intermittent and chronic in nature.
②Symptomaticintestinal amoebiosis
Non-dysenteric colitis: Itis a well recognised condition. It is usually chronic. Symptomatology consists ofintermittent diarrhoea, abdominal pain, flatulence and loss of weight. Thesecases have less colonic inflammation and small amoebic ulcers, amoebae in theirstool and associated antibodies in the serum of the patient. They respond wellto treatment with anti-amoebic drugs.
Acute amoebic dysentery: Itis the common form of invasive intestinal amoebiasis. The condition ischaracterised by the presence of blood and mucus in the stool, accompanied byabdominal pain, tenderness, tender hepatomegaly (肝脾腫大) and rectal tenesmus. Fever is uncommon, present in less thanone-third of the cases.
The condition can be differentiated from that of bacillary dysentery bythe demonstration of RBCs, Charcot-Leyden crystals and haematophagous amoebictrophozoites in the amoebic dysenteric stool.
③Complicationsof symptomatic intestinal amoebiasis: Thick megacolon (巨結(jié)腸) occurs in less than 0.5 percentcases. It is resistant to treatment with anti amoebic drugs, hence requirescolectomy.
Fuhninant amoebic colitis (阿米巴性結(jié)腸炎) has a high mortality and tends to occur more in pregnant women,malnourished persons and persons receiving corticosteroids (皮質(zhì)類(lèi)固醇). The onset is abrupt withhigh fever, widespread abdominal pain, leucocytosis (白細(xì)胞增多), profuse bloody ,mucosal diarrhoeawith tenesmus (里急后重). The patientshave necrotic involvement of their colon. Colonic perforation and haemorrhagefrequently occur in this condition.
Amoeboma (阿米巴腫) is a pseudo-tumoral condition.Lesion may be single or multiple and occurs commonly in the colon, caecum orrectum. Anti-amoebic antibodies are present in the patient serum.
Complicated intestinal amoebiasis:This condition includes peritonitis, perianal ulceration, urogenital infection,colonic stricture, intussusception (腸套疊) and haemorrhage. These complications relatively are uncommon.
2) Extra-intestinal amoebiasis(腸外阿米巴病)
Clinical manifestations ofextra-intestinal amoebiasis dependsupon the organ involved. It can be Hepatic amoebiasis, pulmonary amoebiasis, cerebralamoebiasis, genitourinary amoebiasis, and splenic amoebiasis.
①Hepatic amoebiasis (肝阿米巴病) begins with the hepatic involvement (non suppurative amoebic hepatitis) and progress to form suppurative lesions in the liver(amoebic liver abscess).
②Pulmonary amoebiasis (肺阿米巴病): It is the most commoncomplication (并發(fā)癥) ofamoebic liver abscess and is caused by rupture of a superior right lobe abscessthrough the diaphragm (橫隔膜)into the lung parenchyma. It occurs in 10 to 20 percent of patients.Cough, pleuritic pain and dyspnoea are the common clinical manifestations.
③Cerebralamoebiasis(腦阿米巴病): Amoebicbrain abscess is very unusual. The abscess is single, small and is located inthe cerebral hemisphere. It is difficult to diagnose the condition clinically.
④Genito-urinaryamoebiasis(泌尿生殖系阿米巴病):
⑤Splenicamoebiasis (脾阿米巴病)
DIAGNOSIS
Parasitic diagnosis (病原診斷)
1)Microscopy: 2)Concentration 3)Culture:
Serodiagnosis.
1) Antibody Detection
Molecular diagnosis
Radio diagnosis
EPIDEMIOLOGY
Transmission ways
1) Faecal-oral route 2) Vectors 3) Sexual contact
PREVENTION AND CONTROL
Treating the infected persons
metronidazole (滅滴靈), tinidazole (硝砜咪唑), emetine hydrochloride and2-dehydroemetin. Amoebicides which act only on liver tissue is chloroquine (氯喹). Tetracycline (四環(huán)素)
GIARDIA LAMBLIA (藍(lán)氏賈第鞭毛蟲(chóng))
MORPHOLOGY
Giardia lamblia exists in two stages:trophozoite and cyst.
Trophozooite: It is pear-shaped with broadrounded anterior end and a tapering posterior end (Fig). It measures 9-21µm inlength and 5-15µm in breath and 2-4µm in thick. Dorsal surface is convex (凸起) while ventral surface is concave(凹入). A suckingdisc, the organ of attachment, occupies one-third to one-half of the ventralsurface. Trophozoite is bilaterally symmetrical and has two nuclei, twoaxostyle (軸柱) and fourpairs of flagella. Two median bodies (中體) are present on the axostyle at its origin.
Fig Ⅱ-Ⅵ-1 Giardialamblia Trophozoite
Cytoplasm is uniform and finely granular.The trophozoites are motile due to the presence of four pairs of flagella.
Cyst: the oval cyst measuring 8-12µm inlength and 7-10µm in breath (Fig Ⅱ-Ⅵ-2). A thickwall surrounds it. The cyst consists of cytoplasm, which is finely granular andis separated from the cyst wall by a clear space. This gives an appearance ofthe cyst being surrounded by a halo.
The mature cyst consistsfour nuclei, which may remain clustered at one end or are present in pairs attwo opposite ends. Also it consists of an axostyle and margins of the suckingdisc. The axostyle which is the remains of flagellum is placed diagonally inthe cyst. The four nuclei cyst is the infective stage of G. lamblia.
LIFECYCLE
The life cycle of G. lamblia is simple andis completed in a single host, the man (fig Ⅱ-Ⅵ-2)
Fig Ⅱ-Ⅵ-2 Life cycleof Giardia lamblia (Adapted from parasite image library of CDC, USA)
Cysts are resistant forms and areresponsible for transmission of giardiasis. The cysts are hardy, can surviveseveral months in cold water. Infection occurs by the ingestion of cysts incontaminated water, food, or by the fecal-oral route (hands or fomites). Cystspass through the stomach and excyst to trophozoites in the duodenum within 30minutes of ingestion, each cyst produces two tetranucleate (四核的) trophozoites. Acidity ofgastric juice favours the process of excystation. In duodenum and jejunum, thetetranucleate trophozoite multiply asexually by binary fission therebyproducing a large numbers of daughter trophozoites. Trophozoites browse on themucosal surface, to which they are attached by an oval sucker. When theintestinal contents leave the jejunum and begin to lose moisture, thetrophozoites retract their flagella, cover themselves with a thick wall andencyst. These encysted trophozoites undergo another phase of nuclear divisionand produce four-nucleated mature cysts. The four nucleated mature cysts arethe infective forms of the parasites, they are excreted in faeces and the cycleis repeated.
PATHOGENESIS AND SYMPTOMS
Giardia lamblia inhabits the duodenum (十二指腸) and upper ileum (回腸). The trophozoites may remainattached to the intestinal mucosa and rarely invades the submucosa.
As few as 10-25 cysts can cause giardiasis (賈第鞭毛蟲(chóng)病). Malabsorption (吸收障礙) of fat and carbohydrates inchildren and diarrhoea, are important clinical manifestation. The precisemechanism for these changes is not clear. The pathogenic mechanisms may bemechanical blockage of the intestinal mucosa, or competition for nutrients, orinflammation of the intestinal mucosa, or bacterial induced deconjugation ofbile salts, and altered jejunal motility with or without overgrowth ofintestinal bacteria and yeast.
In giardiasis the histopathology (組織病理學(xué)) of duodenum and jejunum (空腸) are highly variable and mayrange nearly from normal to markedly abnormal. Most commonly, there isshortening of microvilli (微絨毛) and elongation of crypts. The brush border of the absorptive cellsare damaged Giardia mostly are found attached to the lining of the epithelialbrush border.
The clinical features vary fromasymptomatic carriage to severe diarrhea and malabsorption. Majority ofinfected persons in the endemic area, are asymptomatic. Acute giardiasisdevelops after an incubation period of 5 to 6 days and usually lasts 1 to 3weeks. Symptoms include diarrhea, abdominal pain, bloating (胃氣漲), nausea (惡心), and vomiting.
In some patients, the infection progress toa chronic disease. In chronic giardiasis the symptoms are recurrent andmalabsorption and debilitation may occur. The condition frequently isassociated with malnutrition and stunted growth in pre-school children.
DIAGNOSIS
Laboratory diagnosis is based onparasitological methods and to a less extent on serological methods.
Pathogenic diagnosis
1) Fecal examination: Giardiasis isdiagnosed by the identification of cysts or trophozoites in the feces, usingdirect mounts as well as concentration procedures. Repeated samplings may benecessary. In acute giardiasia, motile trophozoites are demonstrated in thedirect wet mount of liquid stool. The cysts are demonstrated in the semiformedstool. The stool specimens are examined either fresh or in case of delay. Afterpreservation by formalin (福爾馬林) or polyvinyl alcohol, and subsequent staining by trichrome (三色) or iron-haematoxylin method.Concentration of stool byformalin-either or zinc sulphate method increase the yield of parasites.Inchronic giardiasis cysts often are excreted intermittently. Hence examinationof at least three stool specimens collected at an interval of 2 days, helps inthe detection of parasites
2) duodenal contents or bile examination:microscope examination of duodenal contents or bile is carried out, when therepeated stool examination is negative but giardiasis is still suspected. Threemethod are used in collecting duodenal contents:
① String testor Entero test (腸檢膠囊法)：It is a gelatin capsule (膠囊) which contains a nylon string atone end. The capsule is swallowed by the patient and the free end of the stringis fixed at the mouth. In the stomach, the capsule is dissolved and the stringremains in duodenum and jejunum. After overnight incubation, the string isremoved, the bile stained mucus is collected on the glass side and examinedmicroscopically for trophozoites.
② Duodenalaspiration(十二指腸引流): it isalso collected to demonstrate trophozoites.
③ Jejunalbiopsy (空腸活檢): It isperformed to demonstrate trophozoites but indicated only in very serious cases.
2). Immunological methods:
Alternate methods for detection includeantigen detection tests by enzyme immunoassays, and detection of parasites byimmunofluorescence. Enzyme-linkedimmunosorbent assay (ELISA) and indirect fluorescent antibody (IFA) are usefulin seroepidemiological studies. These methods detect anti-Giardia antibodies inserum, which remain elevated for a longer period.
EPIDEMIOLOGY
PREVENTION AND CONTROL
Ⅶ TRICHOMONAS VAGINALIS (陰道毛滴蟲(chóng))
MORPHOLOGY
Trichomonas vaginalis only exists introphozoite stage. Cystic stage is absent. Trophozoite inhabit the vagina infemale, the prostate (前列腺) and seminal vesicles in male and urethra (尿道) in both sexes.
LIFE CYCLE
PATHOGENESIS AND SYMPTOMS
irritation, dyspareunia, disagreeable odour and dysuria (排尿困難). The acute stage may last fora week or month and often varies in intensity. It may become severe followingmenstruation. Vaginitis (陰道炎) with a purulent (含膿的) discharge is the prominent symptom, and can be accompanied byvulvar and cervical (子宮頸的) lesions, abdominal pain, dysuria and dyspareunia. The vaginalsecretions are liquid, greenish or yellow and are present on the urethralorifice (尿道口),vestibular glands and clitoris. It contains large numbers of Trichomonas andleucocyte. The incubation period is 5 to 28 days. In men, the infection isfrequently asymptomatic; occasionally, urethritis, epididymitis (附睪炎), and prostatitis (前列腺炎) can occur.
Persistent or reccuring nonspecificurethritis is the main clinical presentation in symptomatic cases.Infection appears to beself-limiting in many of the male possible due to trichomonicidal action of theprostatic fluid or flushing out of the flagellate mechanically from urethraduring micturition (頻尿).
DIAGNOSIS
EPIDEMIOLOGY
PREVENTION AND CONTROL
ⅧPLASMODIUM
P. falciparum(惡性瘧原蟲(chóng)), P. vivax(間日瘧原蟲(chóng)), P. ovale(卵形瘧原蟲(chóng)) and P. malariae(三日瘧原蟲(chóng)).
MORPHOLOGY AND LIFE CYCLE
1) Exo-erythrocytic stage(紅外期): sporozoites (子孢子)into the human host.
tachysporozoite (速發(fā)型子孢子)
bradysporozoite or hypnozoites ( 遲發(fā)型子孢子，休眠子).
undergoes EE schizogony (紅外期裂體增殖).
In P. vivax, hypnozoites (休眠子)
Relapse (復(fù)發(fā))
② Erythrocyticstages(紅細(xì)胞內(nèi)期)
① Trophozoites (滋養(yǎng)體):
ring forms (環(huán)狀體). pigment granules of hemozoin (瘧色素) 、red-staining Schüffner’s dots (薛氏點(diǎn))
②ErythrocyticSchizonts（紅內(nèi)期裂殖體):
Gametocyte (配子母細(xì)胞):
macrogamonts (macrogametocytes，大配子母細(xì)胞，雌配子母細(xì)胞) and
microgamonts(microgametocytes，小配子母細(xì)胞，雄配子母細(xì)胞).microgametes (小配子). oocyst (卵囊).
salivary gland (唾液腺), sporozoites enter its channelsand can be injected into a new host at the next feeding.
FigⅡ-Ⅷ-7 The lifecycle of Plasmodium
(Adapted from parasite image library of CDC, USA)
PATHOGENESIS AND CLINICAL MANIFESTATIONS
Incubation period (潛伏期)
Malarial paroxysm (瘧疾發(fā)作)
Relapse and Recrudescence in malarial infections (復(fù)發(fā)和再燃)
Anemia (貧血)
Complications of malaria (瘧疾并發(fā)癥)
Falciparummalaria (惡性瘧) is alwaysserious, and sometimes severe complications are produced. The most common ofthese is cerebral malaria (腦型瘧), which may account for 10% of falciparum malaria admitted to thehospital and 80% of such deaths. Cerebral malaria may be gradual in onset, but it is commonly sudden; aprogressive headache may be followed by a coma, an uncontrollable rise intemperature to above 41℃,and psychotic (精神病的) symptomsor convulsions (抽搐), especiallyin children. Death may ensue within a matter of hours. Initial stages ofcerebral malaria are easily mistaken for a variety of other conditions,including acute alcoholism, usually with disastrous consequences.
Tropical splenomegaly syndrome (TSS，熱帶綜合巨脾癥)
Congenital malaria (先天性瘧疾)
Transfusion malaria (輸入性瘧疾)
DIAGNOSIS
1)Collection ofblood: Peripheral blood should be collected before starting treatment withantimalarials. It can be collected any time during the fever. Timing of collectionof the blood is less important although a high density of malaria parasitesappear in circulation during paroxysm. More important is the frequent ofexamination of blood smear. Smears should be examined at least twice dailyuntil parasites are detected.
2)Microscopy examination: both thick and thin smears
Quantified buffy coat (QBC) technique （血沉棕黃層定量分析法)
Immunodiagnosis
1) Detection of an antigen (histidine richprotein-2, HRP-2)
2) Detection of antibodies
Molecular diagnosis
Polymerase-chainreaction (聚合酶鏈反應(yīng)，PCR)
EPIDEMIOLOGY
PREVENTION AND CONTROL
ⅨTOXOPLASMA GONDII (剛地弓形蟲(chóng))
opportunistic protozoan (機(jī)會(huì)致病原蟲(chóng)).
MORPHOLOGY
LIFECYCLE
Fig Ⅱ-Ⅸ-3 Life cycleof Toxoplasma gondii (Adapted from parasite image library of CDC, USA)
PATHOGENESIS AND CLINICAL FEATURES
Congenital toxoplasmosis (先天性弓形蟲(chóng)病)
Congenital toxoplasmosis results from anacute primary infection acquired by the mother during pregnancy. Transplacental(經(jīng)胎盤(pán)的) transmissionfrom a chronic infection does not occur.
Congenital toxoplasmosis occursapproximately in one-third of infants born to pregnant women, who acquire theinfection during first trimester of pregnancy. In pregnancy, abortion, death inutero, or severe neurological/ocular manifestations (chorioretinitis),hydrocephalus (腦積水),convulsions (抽搐),intracerebral calcifications (腦石灰化), etc.) may result. Infection of the foetus (胎兒), during last trimester ofpregnancy, is more likely to be mild or asymptomatic at birth. Asymaptomaticinfection at birth, however, may manifest as several sequalae of infectionduring the later life of the child.
The incidence and severity of congenitaltoxoplasmosis vary with the trimester during which infection wasacquired. Because treatment with leucovorin of the mother may reduce theincidence of congenital infection and reduce sequelae (后遺癥) in the infant, prompt andaccurate diagnosis is important.
Acquired toxoplasmosis (獲得性弓形蟲(chóng)病)
Acquired infection with Toxoplasma inimmunocompetent (免疫活性的) personsis generally an asymptomatic infection. However, 10% to 20% of patientswith acute infection may develop cervical lymphadenopathy (淋巴節(jié)病) and/or a flu-likeillness. The clinical course is benign and self-limited; symptoms usuallyresolve within a few months to a year. Immunodeficient patients oftenhave central nervous system (CNS) disease but may have chorioretinitis (脈絡(luò)視網(wǎng)膜炎), or pneumonitis (肺炎). In patients with AIDS,toxoplasmic encephalitis (腦炎) is the most common cause of intracerebral mass lesions and isthought to be caused by reactivation of chronic infection. Toxoplasmosis inpatients being treated with immunosuppressive drugs may be due to either newlyacquired or reactivated latent infection.
Occular tocoplasmosis (眼弓形蟲(chóng)病)
Acute infection of eye begins as single ormultiple foci of necrosis (壞疽) of retina (視網(wǎng)膜) with severe inflammation and exudation into the vitreous (玻璃體). Granulomatous inflammation ofchoroids (脈絡(luò)膜) occurssecondary to necrotising retinitis (視網(wǎng)膜炎). Both the tachyzoites and tissue cysts are found in the retinallesions.
Infection in the immunocompromised host
All types of T. gondii infections thatoccur in the immunocompetent hosts, are also seen in the immunocompromisedhosts. The infection is more serious in immunosuppressed patients receivingimmuno-suppressive therapy for malignancies (惡性腫瘤); or persons receiving organ transplantations (器官移殖) and AIDS.
Infection of the centralnervous system especially, toxoplasmic encephalitis is one of the most commonlyrecognized manifestation of the infection in patients with AIDS. Unless theimmune status of the host is restored, the disease progresses rapidly and deathis the frequent out come of the condition.
DIAGNOSIS
Pathogenic diagnosis:
1) Observation of parasites in patientspecimens,
2) Isolation of parasites from blood orother body fluids,
Serological diagnosis
1) Antibody detection:.
Dye test
2) Antigen detection
Molecular diagnosis
Detection of parasitegenetic material by PCR, especially in detecting congenital infections inutero.
EPIDEMIOLOGY
PREVENTION AND CONTROL
ⅩCRYPTOSPORIDIUM (隱孢子蟲(chóng))
MOPHOLOGY
LIFE CYCLE
PATHOGENESIS AND SYMPTOMS
diarrhea.
DIAGNOSIS
1)Microscopy examination:
2)Acid-faststaining methods:
Histopathological diagnosis
Serodiagnosis
EPIDEM1OLOGY
PREVENTION AND CONTROL
ⅪPNEUMOCYSTIS CARINII (卡氏肺孢子蟲(chóng))
MORPHOLOGY
Pre-cyst: It is an intermediate stage between the trophozoite and cyst.It is oval in shape and measures 4-6 µm in diameter. It lacks pseudopodia.Typically. it is surrounded by athick limiting layer or cell wall. Periodic-acid schiff (PAS) and silvermethenamine stain clearly the cell wall. It is difficult to demonstrate thisstage in the tissue.
Cyst(Fig2): It is spherical. 5-8 µm indiameter and is surrounded by a 70-140 nm thin cell wall. A mature cystconsists up to eight daughter forms or extra-cystic bodies called
sporozoites. The sporozoites are spherical,crescent-shaped, measure1-1.5 µm in diameter. Each sporozoite consists of anucleus, mitochondria, ribosomes and endoplasmic reticulum.
The cyst is the diagnostic form of theparasite and is easily recognisedby staining with
LIFE CYCLE(FigⅡ-Ⅺ-3)
Fig Ⅱ-Ⅺ-3 Life cycleof Pneumocystis carinii
PATHOGENESIS AND CLINICAL MANIFESTATION
P. carinii inhabits the lung alveoli. In man and other animalspecies, it causes disease by attaching itself to Type-1 alveolar epithelialcells. The specific factors involved in the process of attachment have not beenrecognised. The organism lives on the lining layer of the alveoli. It has beendemonstrated that surface of the organism and alveoli epithelial cells areclosely apposed to each other without any fusion of the cell membrane orchanges in the intra-membranous particls.
The lungs, in pneumocystosis(肺孢子蟲(chóng)病) inhumans are consolidated and appear reddish grey at necropsy (尸檢). Histologic studies of the lungshows the alveoli to be completely filled with pink frothy honey combedmaterials and a large number of P. carinii
Infected infants showextensive plasma cell infiltration of the alveolar space but immuno-suppressedchildren and adults do not show these changes, instead they show onlyintestinal thickening.
P. carinii rarely causessymptomatic disease in healthy individuals. It causes diffuse pneumonia only inimmunocompromised hosts. In these hosts, the organism as well as the diseasealways remain localised to the lungs.
The severity of clinicalmanifestations, to some extent, depend on the age of the host as follows:
Epidemic or infantile pneumoeystosis (流行型或嬰兒肺孢子蟲(chóng)病): This occurs inpre-mature, malnourished (營(yíng)養(yǎng)不良) and debilitated (虛弱) infants. Incubationperiod varies from 1 to 2 months. The symptoms of P. carinii pneumonia (PCP)include dyspnea (呼吸困難),non-productive cough (干咳), and fever. Chest radiography demonstrates bilateral infiltrates. In1 to 4 weeks, respiratory manifestations become well marked. The condition maylast 4 to 6 weeks and shows a mortality of 25 to 50 percent.
Sporadic pneumocystosis (散發(fā)型肺孢子蟲(chóng)病): P. carnii produces sporadicpneumocystosis in immunocomprornised children and adults with acquiredimmunodeficincy syndrome (AIDS), or in persons receiving immunosuppressivetherapy for the treatment of malignant conditions, organ transplantation, etc.
The clinical manifestations are similar to that of epidemicpneumocystosis except that the onset of sporadic pneumocystosis is abrupt.Course of the disease is rapid and begins with fever, tachypnoea andrespiratory distress. Extrapulmonary lesions occur in a minority (<3%) ofpatients, involving most frequently the lymph nodes, spleen, liver, and bonemarrow. Typically, in untreated PCP increasing pulmonary involvement leads todeath. The condition has a high mortality of 90-100 percent.
The pathogenesis of pneumocystosis in AIDS and other immunodeficiencydisease still remains unclear.It may be due to simple reactivation of latentinfection or additional exposure to exogenous sources of the organism.
DIAGNOSIS
1) Open lung biopsy.
2) Percutaneous needle biopsy or needle aspirationof the lung.
3) Bronchoalveolar biopsy andbronchoalveolar lavage.
Serodiagnosis
Chest x-ray:
EPIDEMIOLOGY
Transmission :
P. carinii occurs in following ways:
1) Man-to-man transmission:.
2) Congenital transmission occurs rare.
1) Premature malnourished infants;
2) Children with primary immunodeficiency.
3) Patients receiving immuno suppressivedrugs such as corticosteroids for treatment of malignancies, organtransplantations and other diseases; and
4) Protein malnutrition.
TREATMENT AND CONTROL
Pentamidine(戊烷脒), trimethoprim（甲氧芐氨嘧啶) and sulfamethoxazole（新諾明)
Section III TREMATODES（吸蟲(chóng))
I. INTRODUCTION
SPECIES
LIFE CYCLE
Typical Life Cycle includesexual generation（有性生殖) andasexual generation(無(wú)性生殖) (Fig Ⅲ-Ⅰ-1).
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Fig Ⅲ-Ⅰ-1 An example oftrematode life cycle
MORPHOLOGY
Despite superficial differences, themorphology of the various groups of digenetic trematodes is basically uniform.They characteristically flat, leaf like, hermaphrodite（雌雄同體)organisms except for theschistosomes which have a boat shaped male and a cylindrical female. One ormore muscular suckers（吸盤(pán)) are always present on the ventral surface(usually possess apowerful oral sucker that surrounds the mouth, and most also have a midventralacetabulum（腹吸盤(pán)) orventral sucker（腹吸盤(pán)).Reproductive system is highly developed. Excretory and nervous are present.
The eggs of trematodes are operculated（有蓋的) except for schistosomes.
Tegument（體壁組織):
Digestive system:.
Reproductive system: Most trematodes arehermaphroditic（雌雄同體的) exceptschistosoma. Male reproductive system consists of testis, vas efferens（輸出管)，vas deferens（輸精管), seminal vesicale（儲(chǔ)精囊), prostatic gland（前列腺), ejaculatory duct（射精管) or cirrus（陰莖), and cirrus pouch（陰莖囊) etc. Female reproductivesystem consists of ovary（卵巢),oviduct（輸卵管),ootype,（卵模) Mehlis’ gland（梅氏腺), seminal receptacle（受精囊), Laurer’s cana l（勞氏管), vitellaria（卵黃腺), vitelline duct（卵黃管), common vitelline duct（總卵黃管), vitellaria reservoir（卵黃囊), uterus（子宮) and metraterm（子宮末端) etc.
Excretory system It consists of flame cells(焰細(xì)胞)， collecting tutules（集合管) and excretory bladder(排泄囊). These flame cells provide the basis for the identification of thespecies. (Fig Ⅲ-Ⅰ-2)
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II CLONORCHIS SINENSIS（華支睪吸蟲(chóng))
MORPGOLOGY
Adult worm.. Mature egg Theeggs are flask-shaped, operculated and relatively smaller in size, and measure 29 ×17mm. They areyellow-brown(bile stained), containing a well-developed miracidium, andpossessing a small knob at the posterior end giving an appearance of a electricbulb..
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Fig Ⅲ-Ⅱ-1 Egg ofClonorchis sinensis
LIFE CYCLE
Fig Ⅲ-Ⅱ-3 Life cycle of Clonorchis sinensis (from Parasite image library ofCDC, USA)
In the first intermediate host Eggs are hatched（孵出) into miracidium after beingeaten by a suitable snail, then develop into a sporocyst（胞蚴); sporocyst transforms intoredia（雷蚴); rediaproduce cercariae（尾蚴) with longtail.
In the second intermediate host: Whencontacting fish or crustaceans in freshwater, the cercaria will bores throughthe skin, coming to muscle and encysting (metacercaria).
First Intermediate host: fresh-water snailseg. Parafossarulus striatulus(紋沼螺)，Alocinmalongicornis(長(zhǎng)角涵螺),Bithynia fuchsianus(赤豆螺).
Second intermediate host: fresh-water fishi.e. Ctenopharyngodon iddellus(草魚(yú)),Pseudorosbora parva(麥穗魚(yú)) et al.
PATHOGENESIS AND CLINICAL MANIFESTATION
The basic pathogenesis of the infection is erosion（糜爛) of the epithelium（上皮) lining the bile ducts, whichresults from mechanical irritation caused by flukes and toxic substances thatmay be produced by them. Because flukes prefer to reside in the second-orderbile ducts, the pathological changes usually appear in the second-order bileducts. But in heavy infection they are found throughout the biliary system,including the gallbladder（膽囊), and sometime in the pancreatic duct. Flukes feed on secretionsfrom the bile duct mucosa. They cause low-grade inflammatory changes of biliarytree, proliferation of the biliary epithelium, and progressive portal fibrosis.In light infection, the pathological changes is not significant; but heavyinfection will lead the bile ducts to gradual enlarging and thgydjdsj.org.cn/shiti/ickening. Thereis obstruction of the biliary tract by the worm bodies, which leads to bileretention, and fibrosis proliferation in the wall of the tract. In late stagewith complication, the change of liver parenchyma（肝實(shí)質(zhì)) are present, and liver function are interfered. Some research datashowed that there was the relationship between clonorchiasis and biliary tractcancer, liver cancer.
Acute clonorchiasis occurs one to three weeks after the ingestion ofencysted metacercariae. There many be fever, chills, abdominal pain, diarrhea,tender hepatomegaly, and mild jaundice. The white blood cell count is raisedwith marked eosinophilia, and serum alkaline phosphataes, SGOT,and SGPT areelevated. The clinical presentation is often confused with acute viralhepatitis and seldom recognized. The history of eating raw fish in the endemicarea and the eosinophilia should suggest the diagnosis.
The majority of people with C.sinensis intheir stools have no symptoms. The biliary system is blocked by numerous flukesand becomes secondarily infected. The flukes occasionally block the pancreaticducts and induce pancreatitis（胰腺炎). Cholangiocarcinoma（膽管癌) is a late complication of chronic clonorchiasis. Clonorchiasis hasno causal relationship with hepatocellular cancer. Some advanced cases haveserious complications such as cirrhosis of the liver and ascites.
DIAGNOSIS
1) Parasitological examination
EPIDEMIOLOGY
PREVENTION AND CONTROL
Praziquantel（吡喹酮)
III FASCIOLOPSIS BUSKI（布氏姜片蟲(chóng))
MORPHOLOGY
Adult worm
Egg
Fig Ⅲ-Ⅲ-1 The egg ofFasciolopsis buski
LIFE CYCLE
Fig Ⅲ-Ⅲ-2 Life cycle of Flasciolopsis buski (fromParasite image library of CDC, USA)
PATHOGENESIS AND CLINICAL MANIFESTATION
diarrhea with hunger pains, simulatingpeptic ulcer（消化性潰瘍). Ininfected children these clinical manifestation such as weight loss, edema andanaemia（貧血) arefound.
DIAGNOSIS
Specific diagnosis can be made bydemonstrating the characteristic eggs and or adult flukes in the feces. Theeggs must be distinguished from those of other species such as Echinostoma sp.,Fasciola hepatica and F.gigantica.
EPIDEMIOLOGY
Distribution
Human are infected by eating raw stems,leaves, and pods of water plants.
PREVENTION AND CONTROL
praziquantel（吡喹酮)
IV PARAGONIMUS WESTERMANI（衛(wèi)氏并殖吸蟲(chóng))
MORPHOLOGY
Adult worm ( hermaphrodite雌雄同體)
Egg than 10 vitellinecells.
Fig Ⅲ-Ⅳ-1The egg ofParagonimus westermani
LIFE CYCLE
Fig Ⅲ-Ⅳ-1 Life cycleof Paragonimus westermani (from Parasite image library of CDC, USA)
PATHOGENESIS AND CLINICAL MANIFESTATION
Pathological changes in host caused byphysical trauma（損傷) of youngflukes or adult worms' migration and lodge in the tissues, and chemical damagesof flukes' toxins The process of the pathological changes may be divided intoan early or acute stage, and late or chronic stage.
The acute stage Caused by invasion and migrationof the young flukes, symptoms appear several days or one month after eating rawcrab with metacercariae. Becausethe metacercariae excyst in the small intestine, and penetrate through its wallas well as other organs, hemorrhage in the tissue is a common pathologicalchanges. The symptoms have fever, diarrhea, abdominal pain, chest pain or tightsensation, cough and eosinophilia etc.
The chronic stage The stage is divided intoabscess, granuloma（肉芽腫) ,and Fibrous scar（纖維瘢痕).
1) Abscess
2) Granuloma
3) Fibrous scar
① Pulmonaryparagonimiasis:
② Cerebralparagonimiasis:
③ Liverparagonimiasis:
④ Cutaneousparagonimiasis:
DIAGNOSIS
Definitive diagnosis of pulmonary paragonimiasis depends on themicroscopic demonstration of characteristic opereculated eggs in the sputum orfaeces.
Immunodiagnostic tests
X-ray examination of chest /CT
EPIDEMIOLOGY
PREVENTION AND CONTROL
V SCHISTOSOMA JAPONICUM（日本血吸蟲(chóng))
INTRODUCTION
dioecious（雌雄異體的) trematods
The three main species infecting humans areSchistosoma haematobium（埃及血吸蟲(chóng)), S. japonicum（日本血吸蟲(chóng)), and S. mansoni（曼氏血吸蟲(chóng)). Two other species, more localized geographically, are S. mekongi（湄公血吸蟲(chóng)) and S. intercalatum（間插血吸蟲(chóng)). S.japonicum is the mostpathogenic（致病性的) of allthe human schistosome species.
MORPHOLOGY
Adult Worm
Eggs : They are 89 μm in long and 67μm wide, oval and possess a lateralsmall rudimentary knob（小刺) or delicate spine without operculum . There is a mature eggs in thefeces with miracidium in the egg.
It is about 99μm in long and 35μm wide, the body like veritablespinning ball with cilia（纖毛).
Cercaria Cercaria is consist of abody, a tail and a pair of furcae（分叉). The body is 100-150μm long, tail 140-160μm long, and furca 50-70μm long. The oral sucker is comparatively large, and the ventral suckeris small. The body covere with minute spines. Four types of glands open throughducts at the anterior margin of the oral sucker.
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Fig Ⅲ-Ⅴ-1 Differentdevelopment stages of Schistosoma
LIFE CYCLE
Fig Ⅲ-Ⅴ-2 Life cycle of Schistosoma (from Parasite image library of CDC,USA)
The life span of adult worms is usually 4.5years.
PATHOGENESIS AND CLINICAL MANIFESTATION
Eggs deposited by S.japonicum adult female worms are the chief causeof tissue damage, consisting of an inflammatory granulomatous reaction andpseudotubercle formation followed by fibrosis and the sequel of the disease syndromes.But, besides eggs, other developmental stages of schistosome such as cercariae,schistosomule, adult worm can also caused pathological changes in host.
Cercariae
Adult worms
Eggs Eggs with miracidium canrelease some antigenic and enzymatic secretions, which can induce agranulomatous cell-mediated responses of lymphocytes, macrophages andeosinophils, about 100 times the volume of the egg.. The formation of granulomais closely related to development of eggs. As eggs is not mature, no inflammatoryreaction or light reaction appears around the eggs. Because S.japonicum eggswere deposited in cluster, the volume of egg-granuloma is larger in which abouthalf the cells are eosinophils and some cells is plasmacyte(漿細(xì)胞). Meanwhile, antigen-antibodycomplex response named Hoeppli phenomenon appears around eggs.
In summarizing the recent research resultsconcluded" T-cells are of major importance for the formation of largegranuloma around the eggs of S.japonicum like S.mansoni, but modulation of sizeof granuloma is primarily antibody medicated." So the mechanism of granulomatousformation is considered to be VI type delay hypersensitivity.
Following the progress of egg-granuloma,miracidium in egg is to be died and egg is to be calcified, then fibroblastscluster and synthesize collagen. The granulomatous formation transit to fibroustissue, than the permanent fibro-changes due to schistosoma infection wasestablished. Late in the disease, periportal pipestem fibrosis and fibrosis inintestinal walls may result in a clinical picture of cirrhosis, includingportal hypertension（門(mén)脈高壓) and splenomegaly（脾腫大). So the most important pathological changes in the liver are noticein the portal trials, widening of portal trials, fibrosis, and numerous newcapillaries in the fibrosis portal tissues are seen. Apart from the portalsystem, egg granulomatous lesions have been found in lungs, brain, the skin,breast, kidney, ureter and reproduction organs of both sexes etc. Although S.japonicumegg are rarely in endocrine glands, the infection itself, but not the eggdeposition, can cause schistosomiasis dwarfism. In these patients, body growthand development are retarded and significant pathological changes are apparentin the skeleton, endocrine glands as well as reproductive organs.
CLINICAL PRESENTATION
The main clinical finding include weakness, abdominal pain,diarrhoea, hepatomegaly and splenomegaly etc.
In generally,schistosomiasis can be divided into three phases,--acute phase, chronic phaseand late phage.
Acute stage Penetration of the skin bycercariae may appear cercariaedermatitis with local pruritus, erythema and popules. When egg deposition,symptoms with fever, chills, ache and gastrointestinal complaints,hepatomegaly, splenomegaly and eosinophilia etc. Frequently mimicking typhoidfever is commonly seen within a month of infection. In this time, eggs can befound in faces of the patients. Acute cases is usuallyobserved in persons entering the endemic area for the first time.
Chronic stage In endemic areas 90%infected persons are chronic cases of schistosomiasis. Usually more than halfof the chronic cases area symptomatic although stool examination may reveal eggof S.japonicum. The general symptoms: weakness, fatigue, abdominal pain,irregular bowel movements and blood in stool(diarrhoea), hepato-splenomegaly,anemia and emaciation etc.
Late stage In general, some chroniccases with heavy infection will become advanced cases of schistosomiasis( latestage cases) 5 years after infection. Advanced cases has three types,splenomegaly (large spleen), ascites and dwarfism. The common clinical findingare hepato-splenomegaly, ascites, portal hypertension, abdominal collateralvein dilatation and oesophagogastric varices（食道及胃血管曲張). Blood loss due to bleeding of oesophagogastic varices is the majorcause of death in advanced cases.
Ectopic lesion S.japonicum more commonlyinvades the central nervous system and other organs than do the other schistosomes.Ectopic parasite can cause cerebral schistosomiasis, and pulmonaryschistosomiasis etc.
DIAGNOSIS
1) Direct smearsAfter 35-48 days of infection with cercaria, eggs can be found in thefaece by direct smears, the method is simple , but low sensitivity.
2) Hatching ofmiracidium as index ofviable egg
3) Kato-katz's method as quantitative examination,but the sensitivity is low in lightly infection.
4) Microscopical examinationof rectal biopsy themethod is a highly sensitive clinical diagnostic technique, but this invasive procedureis neither simple nor convenient for population-based surveys
Immunodiagnosis It include Skin test(Interdermal test, IDT), antibody detection and antigen detection etc.
1) Interdermal test(IDT) Antigen: adult worm antigen is used for IDT commonly, the sensitivity ismore than 95％, falsepositive rate is about 2％. The test can be done 2weeks after infection, so it possess the values for early diagnosis(or for newinfection) and screening test
2) Antibody detection
① Circumovalpreciptin test(COPT)
antigens: viable eggs
specimen: sera
sensitivity: 97.3％
false positive rate: 3.1％
② Indirecthaemagglutination test(IHA)
antigens: soluble eggantigen(SEA)
specimen: sera
sensitivity: 92.3-100％
false positive: 2％
③Enzyme-linked immunosorbent assay(ELISA)
antigens: SEA/AWA(adult wormantigen)
specimen: sera
sensitivity: 95-100％
false positive rate: 2.5％
3) Antigen detection Unlike antibody detectionwhich can not distinguish between active and past infections, the detection ofcirculating schistosome antigens(CAg) may be a promising approach to thediagnosis of a current infection and the evaluation of drug treatment.
methods: dot-ELISA andsandwich ELISA(double-antibody method)
antibodies: monoclonalantibody(McAb)
sensitivity: 84.5％(29.0-85.0％)
false positive rate: 3.1％ (data from Qu Lizhu 1992)
the negative rate a halfyear after treatment was still 50％
＊ It is considered that the methodsstill need to be improved or modified.
CHEMOTHERAPY
Praziquantel is a antischistosomal agentwith high efficacy and low toxicity. A single dose of 40 mg/kg (50mg/kg) isapplied for treating chronic casesor mass treatment in our country. WHO recommends a dosage of 60mg/kg in 2divided doses give with a 4-h interval on the same day. A total of 120 mg/kg in4-6 days for treating acute cases. Up to now, no deaths due to the drug havebeen reported in more than thousands individuals treated in our country.
EPIDEMIOLOGY
S.japonica is found only in mainland of China,Japan, the Philippians and Indonesia. Japan hascontrolled and eliminated schistosomiasis since 1978.
Distribution In our country schistosomiasis usedto be in 391(381) counties of 12 provinces in the south of China, includingHubei, Hunan, Jangxi, Anhui, Jaingsu, Shanghai, Zhejiang, Fujian, Guangdong, Yunnan,Guangxi, and Sichuan.79 million people resided in endemic areas and 14.8billion m2 snail-ridden areas. After more than 40-year control, schistosomiasishas been eliminated in 5 provinces/municipality/autonomous region, including Shanghai(1985), Guangdong(1985), Fujian, Guangxi, and Zhejiang(1995). Among 391 endemic counties, of 222 countieshave eliminated schistosomiasis, and of 56 controlled transmission ofschistosomiasis.
The current epidemic situation There are still 113 endemiccounties still in China, including marshy type endemic areas (Hubei, Hunan, Jiangxi,Anhui and Jiangsu) and high mountains endemic areas (Sichuan and Yunnan). Upto1995, infected individuals was estimated to be 865084(4.89％ prevalence). Therefore, schistosomiasisis still considered to be a public health problem in China.
Types of endemic areas There are three types ofendemic areas, including Wwater-net regions of plain水網(wǎng)型(e.g., Shanghai, Jiangsu andZhejiang), marshy regions湖沼型(e.g., Hubei, Hunan, Jiangxi, andAnhui), and mountainous and hilly regions山丘型(e.g., Sichuan, Yunnan, Guangdong, Guangxi,and Fujian). In marshyregions including Poyang lake region, Tongtin lake region and beaches ofYangtze river from Hubei to Jiangsu. There are vast snail-infestedareas, which areas is about 82％ total snail-infested areas in China.
Epidemic features
1) Main reservoirs of infection S.japonica is a zoonoses. Infectedlivestock are important reservoirs of infection besides infected persons.Meanwhile 31 species wild mammals e.g. field mice etc are found to be reservoirhosts. Inmost endemic areas, infected cattle or water buffalloes are major reservoirs.
2) Way to infection Contacting infected watercontaining cercaria is only the way(route) to acquire the infection. Ways tocontacting infested water include three types, contacting for production e.g. boating and fishing; for life e.g.washing clothes; for playing e.g. bathing.
3) Susceptible population Humans is a susceptible hostof S.japonicum.. In most endemic areas, both prevalence and intensity increasegradually by age to peak about at 10-20 years of age. But by the beginning thethird decade of life, a slight or moderate decrease in prevalence may be noted;the egg counts are markedly lower in those above 30years of age. The evidence suggested the occurrence of immunity in olderpopulation after repeated infection.
Snail Snail(Oncomelaniahupensis Gredler, 1881) is the only intermediate host of S.japonicum, which normally inhabit flooded areas e.g. thebanks of irrigation ditches and canals, marshes of lakes, and beaches of riveretc. Snail has female and male, female lay eggs in Spring. Baby snail growsunder water, and develop to be adult snail in Autumn. The life span of snail isfrom one to two years. Snails are infested by miracidia and release cercariaduring the periods of immersion in water. So the transmission season is from Aprilto October in China.
Epidemic factors The factors related totransmission of schistosomiasis include natural and social factors. Naturalfactors: environment, temperature, level of water, nature of soil, andvegetation etc. Social factors: economic level, sanitary condition, medicalcare, ways to produce in local and local costumes etc. So environmentmodification, development of economy, health education and nationalprogram of schistosomiasis control will impact on the transmissionsignificantly.
CONTROL AND PREVENTION
Control objectivesIn China,the objective for schistosomiasis control is to control morbidity due toschistosomiasis and to interrupt, in some areas, its transmission. The specificobjectives of the technical strategy are to: a) to reduce morbidity in areas ofthe high endemicity (>15％ prevalence); b) to control morbidity in areas of medium endemicity(areas with prevalence >3％ and 〈15％〉 and c) control morbidity, andtransmission(where appropriate), in areas of low endemicity( areas withprevalence<3％)
Control measures There are different methodsused at different endemic areas.
1) In areas of high endemicity The methods include masschemotherapy, limited snail control by mollusciding with niclosamide,environment modification where appropriate chemotherapy for livestock andhealth education are also preformed.
2) In areas of medium endemicity and of lowendemicity The mainmeasures include selective chemotherapy for human, chemotherapy for livestock,snail control and health education.
3) Individual prevention For the individual orpopulation traveling to endemic areas due to schistosomiasis, avoiding contactwith infested water bodies is the practical preventive measure. If you can notavoid exposure to infested water, Artemether(蒿甲迷) and Artesunate(青蒿琥酯) which are artemisinin(Qin-hao-su)'s derivatives are recommended totake.
Section IV TAPEWORM(絳蟲(chóng))
I. INTRODUCTION
Tapeworms(Cestodes)belong to Class Cestoda（絳蟲(chóng)綱),
Cyclophyllidea（圓葉目)
Pseudophyllidea（假葉目)
MORPHOLOGY
The cestodes are long, segmented and a tape-like worms. They differtrematodes in may ways.
Adult worm Adult worm is flat, long,white or milk white in color. It consists of scolex（頭節(jié)), neck（頸節(jié)), and strobilus（鏈體). Strobilus is a specificstructure of tapeworm, consisting of a linear series of sets of reproductiveorgans of both sexes; each set is referred to as a proglottid or proglottos（節(jié)片). Most tapeworms bear a"head", or scolex, at the anterior end that may be equipped with avariety of holdfast organs to maintain the position of the host in the gut. Thescolex may be provided with suckers（吸盤(pán)), grooves（吸槽), hooks（小鉤), spines（小刺), glands, or combinations of these.
The scolex of Cyclophyllidea（圓葉目) is like ball, in which there are four circular-suckers withrostellum（頂突). Thescolex of Pseudophyllidea（假葉目) is shuttle-like, its holdfast organs are two grooves named bothrium（吸槽).
Commonly, between the scolex and the strobila lies a relativelydifferentiated zone called neck, which may be long or short. At containsgerminal cells that apparently are responsible for giving rise to newproglottids.
Tapeworms are hermaphrodite/ monoecious（雌雄同體)with the exception of a few rare species. Usually each proglottidhas one complete set of both male and female systems. The proglottid nearbyneck is called young proglottid, which reproductive systems is immature. As aproglottid moves toward the posterior end of the strobila, the reproductivesystems mature, which one is called mature proglottid（成節(jié)). As it becomes crowded witheggs, this is gravid proglottid（孕節(jié)).
Reproductive systems Tapeworms are hermaphroditic（雌雄同體的). Usually each proglottid hasone complete set of both male and female systems, but some genera have two setsof each system.
The male organs mature first and producesperm that are stored until maturation of the ovary. The male reproductivesystem consists of one to many testes（睪丸), vas efferens（輸精管), seminal vesicle（儲(chǔ)精囊), deferens cirrus pouch（陰莖囊), and cirrus（陰莖) etc. The female reproductive system consists of an ovary（卵巢) and associated structures,including vitelline follicles（卵黃腺), vitelline duct（卵黃管), uterus（子宮), seminal receptacle（受精囊) and vagina（陰道)etc.
LIFE CYCLE
The development stages ofCyclophyllidea: egg, oncosphere(in intermediatehost), bladder worm（囊蟲(chóng))/coenurus（多頭蚴)/hydatid cyst（棘球蚴) containing proto-scolex （原頭蚴)and alveolar hydatid cyst（泡球蚴)/multilocular hydatid cyst（多房棘球蚴) in the tissues, adult wormin definitive host.
PATHOGENESIS AND PATHOLOGY
EPIDEMIOLOGY
DIAGNOSIS
PREVENTION AND CONTROL
MAIN HUMAN TAPEWORMS
Pseudophyllidea: Spirometra mansoni(曼氏迭宮絳蟲(chóng)),
Diphyllobothrium latum(闊節(jié)裂頭絳蟲(chóng))
Cyclophyllidea: Taenia solium(鏈狀帶絳蟲(chóng))
Taenia saginata(肥胖帶絳蟲(chóng))
Echinococcus granulosus(細(xì)粒棘球絳蟲(chóng))
Echinococcusmultilocularis(多房棘球絳蟲(chóng))
Hymenolepis nana(微小膜殼絳蟲(chóng))
Hymenolepis diminuta(縮小膜殼絳蟲(chóng))
II TAENIA SOLIUM（豬帶絳蟲(chóng)/鏈狀帶絳蟲(chóng))
T. solium called the porktapeworm can cause the infection of T.solium taeniasis（豬帶絳蟲(chóng)病), and its cysticercus（囊尾蚴) cause human cysticercosis（囊蟲(chóng)病). The life cycle of theparasite was first described by Kuchemeister(1855) and Leukart(1856). Hedemonstrated that the larval stage(Cysticercus cellulosae) of the parasite presentin the muscles of the pig is infective to man. It is the only cestode for whichman acts as both the definitive host(harbouring the adult worm) and theintermediate host(harbouring the larva of the parasite).
MORPHOLOGY
Adult worm measures 2 to 4 meters in lengthand has a scolex, neck and segments. Differences between the adult worms ofT.solium and T.saginata are described in the below Table.
1) Scolex hooklets（小鉤), rostellum（頂突). T
2) Neck The neck is short and 5-10 mm long and about one-half as thick ashead.
3) Proglottid The strobila（鏈體) consists of 700-1000 segments
4) Egg The are brown colored,round shaped and measure 31-43 μm in diameter. It are provided with a two layered shell. The outershell is thin, transparent and does not always remain with the eggs. The innerembryophore（胚膜) is athick, brown, roughly structured wall which surrounds the embryo.
Fig Ⅳ-Ⅱ-1 Scolex,mature and gravid proglottids of T. solium Fig Ⅳ-Ⅱ-2 The egg of T. solium
5) Cysticercus cellulosae（豬囊尾蚴)
LIFE CYCLE
Definitive host: Man
Intermediate host: Pig, at time man
Humans is the definitive host as well asintermediate host of T.solium. Adult worm live in the intestine, and fix thewall by its scolex. The gravid proglottids become detached from the strobila（鏈體), usually in groups of three tofive, and are excreted passively in the human feces. The eggs are scattered fromthe proglottids which are damaged or macerated. The T. solium eggs can survive in the environment forseveral months. Pigs are infected after ingestion of the proglottid or eggspresent in an environment contaminated by humans.
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Fig Ⅳ-Ⅱ-3 Life cycle of Taenia solium
The oncosphere（六鉤蚴) leaves the embryophore in thepig intestine and migrates to the tissue; the bladder larva cysticercusdevelops mainly in the muscle tissue and the myocardium but often also in thebrain and liver. The cysticerci become fully grown and invasive for humans 2months after ingestion of the eggs.
A human acquires taeniasisingesting T. solium cysticerci in raw pork. In the human small intestine thescolex attaches itself to the mucosa and within 2 months develops into an adulttapeworm producing eggs. It is reported that T. solium can live more than 25years in humans.
If humans swallow eggs or gravidproglottids, the oncosphere can develops bladder worm like in pig. But itcann't continue to develop adult worm.
PATHOGENSIS AND CLINICAL MANIFESTATION
Both adult andlarvae(Cysticercus cellulosae) are pathogenic.
The adult worm The adult worm occasionallymay cause mild irritation or inflammation of the intestinal mucosa by theirarmed scolex. The clinical manifestation of intestinal T.solium taeniasis isrelatively mild. Vague abdominal discomfort, hunger pangs, and chronicindigestion have been reported but are undoubtedly seen more often in patientswho are aware of their parasitic infection than in those who are not. Moderateeosinophilia frequently occurs.
The larvae or Cysticercus cellulosae The Cysticercuscellulosae frequently cause a serious diseases known as Cysticercosis in man.The number of bladder worms parasitizing in humans range from 1 to thousands.Virtually every organ and tissue of the body may harbor bladder worms. Mostcommonly they are found in the subcutaneous ,connective tissues; followed siteis the eyes, brain, muscles, heart, liver, lungs, and coelom. A fibrous capsuleof host origin surrounds the larvae. The seriousness of the disease dependsupon:
The sites of location of cysticerci, and
Numbers of cysticerci.
Cysticerci can develop in any other organ and issue of man, but arecommonly present in the following sites:
Muscle, subcutaneous tissue and viscera areaffected in disseminated cysticercosis. The viable cysticerci evoke a moderatetissue reaction while the dead cysticerci evoke a strong inflammatory reactionin the tissues.
Eye is affected in ophthalmic（眼的) cysticercosis. The cysticerciare often present in the subcutaneous tissue, vitreous humour（玻璃狀液), anterior chamber（眼前房) of the eye, and
Brain and spinal cord of the centralnervous system are involved in neurocysticercosis. Cystic lesions are usually 2 cm in diameter and found chiefly inthe meninges（腦脊膜),cerebrum（大腦),ventricles and subarachnoid space（蛛網(wǎng)膜下腔), at the base and ventricles of the brain.
Subcutaneous or muscularcysticercosis is usually asymptomatic. The presence of a large number ofcysticerci in the muscles and subcutaneous tissues may cause muscle pain, crampand fatigue.
Neurocysticercosis（腦囊蟲(chóng)病) is the most serious clinicalmanifestation of the condition. The human brain can be invaded by one, byseveral, or even by more than two thousand cysticerci. Some cases have not anysymptoms, but some may die suddenly. Usually its process is slow, the incubationperiod range from one month to one year, but can last 30 years in a few cases.The symptomatogy of cerebral cysticercosis is characterized by three basicsyndromes: convulsions（驚厥), intracrnial hypertension, and psychiatric disorder, occurringseparately or in combination. The prognosis of cerebral cysticercosis is highlyvariable and unpredictable.
Ocular cysticercosis（眼囊蟲(chóng)病) may cause irreparable damageto the retina, iris, uvea, or choroids. This disease constitute about one-fifthof human neurocysticercosis cases. Host reactions to cysticerci vary fromslight to severe inflammation with complication such as chorioretinitis（脈絡(luò)膜視網(wǎng)膜炎), and iridocyclitis（虹膜睫狀體炎).
DIAGNOSIS
Intestinal taeniasis
Cysticercosis
Radio diagnosis: In subcutaneous cysticercosis, plain X-ray of thesoft tissues may show oval or elongated cysts if they are calcified. X-ray ofthe skull may demonstrate cerebral calcification and reveal intracranial(顱內(nèi)) cysticercosis in theneurocysticercosis. CT and MRI(magnetic resonance imaging) are very useful inthe diagnosis of neurocysticercosis. They detect both calcified andnon-calcified cysts and also show intracranial cysts.
Biopsy: the easiest type to diagnose bybiopsy is subcutaneous cysticercosis.
Serological diagnosis: At present,serological examination is considered to be useful for diagnosis. These methodsinclude IHA, ELISA, and Dot-ELISA for detecting specific antibodies.
EPIDEMIOLOGY
PREVENTION AND CONTROL OF CYSTICERCOSIS
Praziquantel
Section V NEMATODE(線蟲(chóng))
I. INTRODUCTION
The nematode belong to the Class Nematoda,which is larger population of invertebrates. It is estimated there are about 10thousand species of the nematode. Most nematodes live in fresh-water, orsea-water, or soil freely( free living, e.g, Caenorhabditis elegans秀麗桿線蟲(chóng)), a few are parasitic.Parasitic nematodes that infect humans have about 10 species, including Ascarislumbricoides（蛔蟲(chóng)), hookworm（鉤蟲(chóng)), filarial（絲蟲(chóng)) and Trichinella spiralis（旋毛蟲(chóng)).
MORPHOLOGY
Structure of the adult pseudocoelom(假體腔)，in which the reproductive system and other structures are found.Sexual dimorphism(dioecious,雌雄異體)
Structure of egg Eggs of parasitic nematodesordinarily consist of three layers enclosing an embryo (卵黃膜或受精膜)that may range from a fewblastomeres to a completely formed larva. Immediately following spermpenetration, the oocyte secretes a fertilization membrane, which graduallythickens to form the chitinous shell/chitinous layer(殼質(zhì)層). The inner membrane, the lipidlayer/ascaroside(脂層或蛔甙層), is formedby the zygote.
Embryo member（受精膜): consist of lipid protein;
Chitonous layer（殼質(zhì)層): consist of chitonous andprotein, and process the function of resisting the mechanic pression;
Lipid layer/ascaroside（脂層或稱(chēng)蛔甙層): consist of lipid proteinand ascaroside, and process the function of regulating.
LIFE CYCLE
The basic process of development includeegg, larva and adult.
nematodes（土源性線蟲(chóng)), such as hookworm. Some parasitic nematodes need intermediate hostto complete the life cycle, these nematodes are called vector-transmissionnematodes or bio-source nematodes（生物源性線蟲(chóng)), such as filaria（絲蟲(chóng)).
CLASSIFICATIONOF PARASITIC NEMATODES
Common human parasitic nematodes belong toClass Nematoda, including Ascris lumbricoides(蛔蟲(chóng)，似蚓蛔線蟲(chóng)), Enterobius vermicularis(蠕形住形腸線蟲(chóng)，蟯蟲(chóng))，Trichuristrichura(毛首鞭形線蟲(chóng)，鞭蟲(chóng))，Ancylostoma duodenale(十二指腸鉤口線蟲(chóng))，Necator americanus(美洲板口線蟲(chóng))，Wuchereria bancrofti(班氏吳策線蟲(chóng)，班氏絲蟲(chóng))，Brugia malayi(馬來(lái)布魯線蟲(chóng)，馬來(lái)絲蟲(chóng))，Trichinella spirialis(旋毛形線蟲(chóng)，旋毛蟲(chóng))。
II Ascaris lumbricoides（蛔蟲(chóng)，似蚓蛔線蟲(chóng))
Ascaris lumbricoides is one of most common human parasites, whichadult worm parasitize in the intestinal tract of human, and cause Ascariasis.
MORPHOLOGY
In Ascris lumbricoides, known as the large intestinal round-worm ofhumans, females may attain a length of 40 cm while male worms may reach 20～35 cm. In both sexes, themouth is surrounded by one dorsal and two ventrolateral lips. The posterior endof the female is straight while that of the male curves ventrally. The femalesis a prodigious egg producer, depositing about 200,000 eggs daily; the uterusmay contain up to 27 million eggs at a time.
The fertilized egg measures 45～75 × 35～50μm, there are three layers in the shell and one embryo cell in theegg. Some time the protein membrane(蛋白膜) may be found outside of egg shell. The shell is relatively thin,hyaline and transparent. The embryonated eggs are infective to human.Unfertilized egg measures 88～94 × 39～44μm, there is no ascaroside in the shell and embryo cell inunfertilized egg.
Fig Ⅴ-Ⅱ-1 Thefertilized egg and unfertilized egg of . Ascris lumbricoides
LIFE CYCLE
The life cycle of Ascris consist of twoparts, one is eggs development in the soil, another adult worms inhabit humansbody.
Adult worms inhabit the lumen of the smallintestine
Fig Ⅴ-Ⅱ-2 Life cycle of Ascarialumbricoides (from Parasite image library of CDC, USA)
PATHOGENESIS AND CLINICAL MANIFESTATION
Migrating larva Minute hemorrhages occur at the penetration sites of the larvae throughthe intestinal wall and into the alveoli of the lungs. During the passagethrough the liver and lungs, the larvae may be immobilized, covered witheosinophile, enveloped in eosinophilic granulomas. Especially in lungs, thepathological changes may be more significant. Larvae from large numbers ofinfective eggs, or repeated ingestion of eggs, produce pathologic changes inthe lungs characterized by a lobular pneumonitis.
Local reactions are usually accompanied bygeneral hypersensitivity reactions such as bronchial asthma（哮喘), transient eosinophilicpulmonary infiltrates(一過(guò)性嗜酸細(xì)胞浸潤(rùn)，肺蛔蟲(chóng)癥,Loeffer’s syndrome). Angioneurotic edema（班尼斯特病或血管神經(jīng)水腫), and urticaria（風(fēng)疹).
Adult worm
1) Intaking nutrients and negatively affectthe absorption
Clinical symptoms include anepithymia（食欲不振)，nausea（惡心)，vomiting（嘔吐)，vague abdominal pains（臍周疼痛)。
2) Allergy The most common skin change isurticaria(風(fēng)疹),itch（皮膚瘙癢)and Angioneurotic edema（血管神經(jīng)水腫).
3) Complication of Ascariasis The adult Ascaris worm is arelatively common cause of severe complications due to its characteristicallylarge size and aggregating and/or migratory activities. The migratration ofadult Ascaris may be promoted by some drugs, including some antihelminthics andthose used for anesthesia, but also by fever and peppery food.
Large numbers of adult worms sometimescause mechanical blockage of the intestine, which produces partial or completeobstruction. The usual site of obstruction is the ileocecal region. Thesymptoms usually start suddenly with vomiting and colicky, recurring abdominalpain; intestinal perforation areless common. Among the most common signs are abdominal distension andtenderness, abnormal abdominal sounds and X-ray evidence of intestinalobstruction.
Ascaris worms can invade the bile duct,pancreatic duct, appendix etc, and cause biliary or hepatic, pancreatic, and appendix ascariasis or ascariasisgranulomas, which occurs most frequently in children. Among the most commoncomplication is biliary ascariasis. The symptoms usually include right upperabdominal pain, which is characterized by a sudden onset, and a very strongintensity. Vomiting with bile-stained gastric contents frequently coexists withthe pain. A typical sign is pain at the pressure point just below the xiphoidprocess（劍突). Seriouscase may occur biliary necrosis or perforation.
DIAGNOSIS
Diagnosis is made by identification of eggsin feces. Because egg production per female is fairly constant, egg counts canprovide reasonably accurate estimates of the number of adult worms present,provided uniform samples are used.
EPIDEMIOLOGY
PREVENTION AND CONTROL
pyrantel pamoate(噻嘧啶) and Mebendazole（甲苯咪唑)
III Trichuris trichiura（毛首鞭形線蟲(chóng)/鞭蟲(chóng))
MORPHOLOGY
Adult worm
Egg
LIFE CYCLE
The life cycle of T.trichiura is simple, complete in a single host, the man. The change of host isneeded for the continuation of species.
Adult whipworms occur primarily in thehuman host’s colon but also inhabit the appendix and rectum. The femaledeposits up to 1000 ～7000 eggs daily; after passing to the exterior in feces, the eggsdevelop slowly in warm, damp/moist soil. An unhatched, infective, third-stagelarva develops in three to five weeks. New human hosts become infected whenthese embryonated eggs are ingested with contaminated food or water or fromfingers. The larvae hatch in the upper portions of small intestine and quicklyburrow into the cells of the intestinal villi, where they mature, undergoingtwo molts in about 3-10days. Subsequently, they migrate to the caecal regionand develop to sexual maturity in 30-90 days from the time the eggs wereingested. Adult worms embed the long, slender, anterior ends of their bodiesdeeply into the colon submucosa. While these worms normally surviveapproximately 3-5 years in the human host.
PATHOGENESIS AND CLINICAL MANIFESTATION
The major pathology resemble that ofinflammatory bowel disease due to mechanical disruption and toxicity of whipworms.The pathological changes include hyperemia(充血)、edema(水腫) or hemorrhage/bleeding(出血). In few cases, there are cellularproliferation（細(xì)胞增生)andthickness of the intestinal wall causing by inflammatory and granulomas .
Most infections are light with no clinicalsymptoms. Chronic infections, however, produce symptoms such as bloody stools/chronicdiarrhea, pain in the abdomen, weight loss, rectal prolapse(直腸脫垂), anemia(貧血). It was reported that 73% ofpersons infected with whipworm were identified to be the cases of chroniccolonitis by fibrescopy（纖維鏡).
DIAGNOSIS
The clinical manifestation are notspecific, so identification of eggs in fecal material constitutes diagnosis. Itis based on the demonstration of the characteristic barrel-shaped eggs in the faecesby light microscopy.
EPIDEMIOLOGY
PREVENTION AND CONTROL
IV ENTEROBIUS VERMICULARIS（蠕形住腸線蟲(chóng)/蟯蟲(chóng))
MORPHOLOGY
Adult worm
Egg The eggsare ovoid but asymmetrically flattened on one side, measuring 50～60×20～30μm ; a colorless, thick shell coversthe larva. The embryonated eggs are infective to humans.
LIFE CYCLE
Life cycle of E.vermicularis is simple and is completed in a singlehost. Man is the natural host. No intermediate.
Fig Ⅴ-Ⅳ-2 Life cycle of (fromParasite image library of CDC, USA)
PATHOGENESIS AND CLINICAL MANIFESTATION
Pinworm are not highly pathogenic as theparasite causes little mechanical injury to the colonic mu and the toxemic orallergic action is disputable. Most of the evident pathological changes due toitching and irritation caused by the migration of gravid females around theperianal, perineal, and vaginal areas. Enterobiasis is usually asymptomatic.Heavy infections in children may also produce such symptoms as sleeplessness,weight loss, hyperactivity, grinding of teeth, abdominal pain, and vomiting.
Gravid females may also migrate up thefemale reproductive tract, become trapped in the tissues, and cause vaginitis(陰道炎), endometritis(子宮內(nèi)膜炎) and granulomata in the uterusand fallopian tubes. They may also migrate to the appendix, the peritonealcavity, or even the urinary bladder.
DIAGNOSIS
The most reliable procedure for finding eggs is to apply a strip ofcellophane tape to the perianal skin, remove the tape, and place it on a cleanmicroscope slide for examination. Negative results from this protocol for sevenconsecutive days constitute confirmation that the patient is free of infection.
EPIDEMIOLOGY
E.vermicularis is one of the most common human parasites.Children,especially of early school-age, are most vulnerable to pinworminfection. The geographic distribution of the worm is global. In Alaskan of USAa 51% prevalence in children was displayed.
In China, enterobiasis cased werefound in all provinces and be recorded in any age group. The infection rate washigher in children and in urban than in adult and in rural areas, respectively.According to a national survey on infection status of intestinal helminthiasisthe infection rate were 30.4%,29.5% and 31.4% in children aged 7-12 years,males and females, as an average, respectively.
Humans is only host of pinworm. Infectionsoccur in one of four ways: (1) retroinfection（逆行感染), when hatched larvae migrate back into the large intestine; (2)self-infection（自身感染), whenthe patient is reinfected by hand-to-mouth transmission; (3) cross-infection（交叉感染), when infective eggs areingested, either with contaminated food or from fingers that have been incontact with contaminated surface or body parts from infected humans; and (4)inhalation of airborn eggs（吸入感染). In household with heavily infected individuals, infective eggshave been found in samples of dust taken from chairs, tabletops, dresser tops,floors, baseboards, etc. In a survey to determine the distribution of airbornpollen in public places, pinworm eggs were found in theaters, not only on armrests and baseboards but also on chandeliers high above the seats; Experimentsshow that at room temperature , eggs survive about 3 weeks.
PREVENTION AND CONTROL
V Ancylostoma duodenale and Necatoramericanus
(十二指腸鉤口線蟲(chóng)和美洲板口線蟲(chóng))
MORPHOLOGY
Adult worm The worms arecylindrical, grayish white and slightly curved. The anterior end of the worm isbent slightly, in the same direction of the body curve and gives in its name“hook worm”. Adults of A. duodenale are somewhat larger than those of N.americanus. Female adults measure about 1 cmlong. The posterior end of the male has an umbrella-shaped bursa(copulatorybursa, 交合傘), withriblike rays（輻肋).The mouthor buccal capsule（口囊) ofA.duodenale has two pairs of curved teeth(鉤齒) on the ventral wall of its buccal capsule, N. americanus has aconspicuous pair of semilunar(半月形) cutting plates（板齒) on the dorsal wall(背側(cè)).
Egg The eggs are oval(56～76×36～40μm) thin–shelled and colourless. These are surrounded by a thin transparent membrane.The eggs usually contain two or four blastomere（胚細(xì)胞)in faeces. When passed in the faeces, these eggs are not infectiveto man and a clear space is always present between the segmented ovum and theegg shell.
LIFE CYCLE
Fig Ⅴ-Ⅴ-3 Life cycleof hookworm (from Parasite image library of CDC, USA)
PATHOGENESIS AND CLINICAL MANIFESTATION
The infection with A.duodenale is more serious than that caused byN. americanus. Pathogenic changes in hookworm infection is the adult worms andless frequently, by the infective larvae.
By adult worm The major pathologicalchanges is caused by the attachment of the adults worms in the small intestineby their buccal capsules. These worms cause considerable loss of blood and tissuefluids, during their feeding on the intestinal mucosa. One A.duodenale adultworm is responsible for loss of 0.15 to 0.26 ml blood per day. One N.americanus adult worm is responsible for loss of 0.02 to 0.10 ml blood per day.The blood loss is caused by:
Ingestion of the blood by the worm.
Seepage （滲出)of the blood around the site of attachment of the worm.
Oozing（滲出)of the blood from the burrowed site previously attached by the worm,and
Anticoagulants(抗凝素) secreted by the buccal capsuleof the worm, which prevent clotting of the blood at the wound site.
Excessive blood loss caused by heavy andprolonged worm infection leads to hypochromic microcytic anaemia（低色素小細(xì)胞性貧血). The anaemia canfrequently become serious and even fatal in the persons with low iron intakeand low level of inor absorption. Loss of protein leads to hypoproteinemia ( 低蛋白血癥)and oedema.（水腫).
The early phase manifests as low-gradefever, anaemia, nausea, vomiting, diarrhoea and abdominal discomfort.Iron-deficiency anaemia and hypoalbuminaemia are major clinicalmanifestation.Development of anaemia depends on the worm load of the intestineand nutritional status of the host. Infection in children is associated withdesire to eat the soil and other unusual substances.
By larva The infective filariformlarvae at the site of the penetration of the skin produce a local reactioncalled ground itch, frequently complicated by secondary bacterial infections.The migration of a large number of larvae, through the lung, produce minutehaemorrhage and infiltration of leucocytes resulting the entrapment of thelarvae in lung tissues. Both eosinophilia and leucocytosis occur at this stage.
Ground-itch is important manifestation inskin phase. In lung phase, fever, cough, dyspn oea（呼吸困難), pharyngitis（咽炎)and occasionally, haemoptysis（咯血)are the important symptoms.
DIAGNOSIS
Eosinophilic leucocytosis（嗜酸性細(xì)胞增多癥) and hypochromicmicrocytic anaemia（低色素小細(xì)胞性貧血) may be suggestive of the condition in the endemic areas.
Laboratory diagnosis It includes parasiticdiagnosis and immunodiagnosis. Parasitic diagnosis is made by demonstration ofthe hookworm eggs in the faeces by microscopy and concentration.
1) Microscopy Direct microscopicexamination of faeces is adequate to detect moderate or serve infections.
2) Concentration Concentration of stool byformalin-ether or simple salt floatation stool is essential to detect lighthookworm infection.
3) Third-stage larvae in the faecalculture
EPIDEMIOLOGY
PREVENTION AND CONTROL
VI Filaria (絲蟲(chóng))
Wuchereria bancrofti(班氏吳策線蟲(chóng)又稱(chēng)班氏絲蟲(chóng)) and Brugia malayi(馬來(lái)布魯線蟲(chóng)又稱(chēng)馬來(lái)絲蟲(chóng)).
MORPHOLOGY
Adult worm Both of filariae aresimilar, such as milk white, threadlike with smooth surfaces , less 1.0mm long. Their mouth with papillae islocated at the top of the head. On the ventrally curved tail of male worm,there are pairs of papillae. Female is larger than male, uterus with embryosand larvae occupies almost the whole body.
Microfilariae Microfilariae withsheaths(鞘) are bluntlyrounded（鈍圓)anteriorend and and pointed tail end. Internal structures can be visualized by the useof fixed stained preparations. In a stained preparation, it shows a centralcolumn of nuclei consisting of few anatomical ”land marks”. These land marksare use to differentiate the Microfilariae of W. bancrofti from B.malayi Theseare :a) nerve ring(神經(jīng)環(huán)), b) body cell (體核), c) tail nuclei(尾核) . The morphological differences of the microfiliariae ofW.Bancrofti from B.malayi are as follows:
LIFE CYCLE
Fig Ⅴ-Ⅵ-2 Life cycle of Wuchereria bancrofti (from Parasite image library ofCDC, USA)
PATHOGENESIS AND CLINICAL MANIFESTATION
Pathogenesis Themicrofilariae is do not harm the human host. Light infections may remainsymptomless but are likely to be associated with an eosinophilia, tropicalpulmonary eosinophilia, TPE). In more intense and repeated infections thepresence of mature worms in the lymphatic vessels and nodes leads to allergicinflammation around the lymphatics（淋巴管) and to temporary lymphatic obstruction（阻塞). Eventually, after repeatedattacks, in some of which secondary bacterial infections may play a part,permanent obstruction of a main lymphatic trunk may be produced. Lymphaticsrupture(破裂) and lymphspills into tissues. Progressive enlargement of the limb or region below theobstruction then follows with thickening and fibrosis of the tissues.
Acute lymphatic pathology The secretions and metabolites ofmicrofilariae and adult worms can causes acute allergic reaction, which belongto type I or type III of hypersensitivity（變態(tài)反應(yīng)). In early stage, there are edema（水腫) and thickening of lymphatic vessels. And then, the wall and tissuearound vessel were infiltrated（浸潤(rùn)) by eosinophils（嗜酸性粒細(xì)胞), plasma cells, lymphocytes, and macrophages which tended to forminto nodules.
Frequent early manifestations of filariasisare fever, lymphangeitis（淋巴管炎), lymphadenitis（淋巴結(jié)炎) and dermatitis（皮炎). The characteristic symptom of lymphangeitis is erythema（紅斑) along the course of inflamedlymphatic called “l(fā)iu huo（流火)” in Chinese.
Chronic lymphatic pathology Chronic lymphatic symptoms mainlyresult in lymphatic obstruction. Adult worms and microfilariae cause .inflammation and allergic reaction, which leads to obstruction of lymphaticvessels. The press of lower lymphatic vessel obstructed become higher, thenlymphatic rupture and lymph spills into tissues. The infected people havedifferent clinical manifestations based on the location of obstruction.
1)Elephantiasis（象皮腫) Elephantiasis isa common symptom of chronic filariasis. Lymphatic rupture and lymph spills intotissues, and then progressive enlargement, coarsening（變粗), corrugation（變皺) and fissuring（裂開(kāi)) of the skin and subcutaneoustissue, with warty superficial excrescences, develop gradually until a legresembles that of an elephant. The name ‘elephantiasis” may also occur in anupper limb.
2) Hydrocele testis（陰囊腫) Obstruction ofspermatic cord(精索) and testislymphatcs may be caused to hydrocele testis. The manifestation is commonlyfound from the patient with W.bancrofti infection.
3) Chyluria（乳糜屎) Obstruction ofObstruction of the abdominal or thoracic lymphatics may be lead to chyluria（乳糜屎), chylous ascite（乳糜性腹水)or a chylous pleural effusion（乳糜性胸腔積液). The manifestation iscommonly found from the patient with W. bancrofti infection.
The interval between infection and theonset of elephantiasis is usually not less than 10 years, after which thecondition tends to be slowly but remorselessly progressive. Gross elephantiasisdevelops only in association with repeated infections in highly endemic areas.
Asymptomatic filariasis Such patients were onlydefined/found by finding microfilariae in the nodes or lung. Most common of thesymptomatic clinical syndromes are recurrent episodes of ‘filarial fever”, thetropical eosinophilia syndrome, higher level of IgE etc.
DIAGNOSIS
The clinical manifestations are suggestivefor filariasis diagnosis. As most of the manifestation are non-specific, thelaboratory diagnosis plays important role.
Laboratory diagnosis include parasiticdiagnosis for microfilariae or adult worm in circulating blood, andimmunodiagnosis for detecting the specific antigens or antibodies in serum ofpatients.
Parasitic diagnosis It is made bydemonstration of the microfilariae in the peripheral blood and rarely, in thechylous urine(乳糜尿)andhydrocele fluid（陰囊積液) and bydemonstration of adult worm。Microfilariae can be demonstrated in the blood by the followingmethods:
1) Thick blood smear Thick blood smear The thick blood smear was made using 60ml blood( 2 to 3 drops of peripheralblood), after drying, then stained with Giemsa. Optimal blood drawing time isfrom 10 PM to 2 AM for W.bancrofti, from 8PM to 4 AM for B.malayi.
2) Other methods for microfilariaedetecting freshblood drop method, concentration, DEC(海群生) provocative test, examination of microfilariae in urine and otherbody fluid.
3) Examination of adult worm The cross sections of adultworms are demonstrated in the biopsy specimens of the enlarged lymph nodesimmediately proximal（近端的) to the affected lymphatic vessels.
Immonodiagnosis Immunodiagnosis methodsplay an important role in the diagnosis of filariasis, especially in the casewith low density of microfilariae states. It is commonly used forepidemiological survey.
Interdermal test (IDT) for screening inpopulation,
Serological tests Detecting for antibodiessuch as IFA,IEST ELISA and IHA and detecting for antigens such as dot-ELISA andSandwich- ELISA.
EPIDEMIOLOGY
Mosquito vectorsThere are more than 10 species of mosquitoes have been proven to besatisfactory intermediate hosts in China. The most important knowvectors in our country are Culex pipiens pallens（淡色庫(kù)蚊) ,Culex fatigans（致乏庫(kù)蚊) and Anopheles sinensis（中華按蚊)for W. Bancrofti and Anopheles anthropophagus（嗜人按蚊), Anopheles sinensis（中華按蚊) and Aedes togoi（東鄉(xiāng)伊蚊) for B. malayi.
PROVENTION AND CONTROL
hetrazan(DEC，海群生/乙胺嗪).
VII Trichinella spiralis（旋毛蟲(chóng))
MORPHOLOGY
Adult worm
Larvae cyst(幼蟲(chóng)囊包) The cyst are found inskeletal muscle commonly, its size is about 0.25～0.5×0.21～0.42 mm. Usually, there ismore than one larvae in a cyst.
Fig Ⅴ-Ⅶ-1 Larvae cyst(幼蟲(chóng)囊包) of Trichnella spiralis
LIFE CYCLE
Fig Ⅴ-Ⅶ-2 Life cycle of Trichnella spiralis (from Parasite image library of CDC,USA)
PATHOGENESIS AND CLINICAL MENIFESTATION
The process of pathological change can be divided three phases.
Invade phase The phase occur within the first weekafter ingestion of infected meat, during the intestinal phase; this phase isassociated with the development of larvae develop into adult. For invading oflarvae and adult worms, the wall of intestine is damaged. Microscopiculceration(潰瘍), mucosalhyperemia（粘膜充血),localized edema（局限性水腫), punctatehemorrhages（出血), andintestinal inflammation may main pathological changes. Gastrointestinal signsand symptoms may be the first evidence of infection, including fever,disgusting, vomiting, abdominal discomfort, diarrhea etc.
Migratory phase This phase, beginning about 7 to 9days after exposure, is associated with penetration of the newborm larvae intomuscle cells, initiating a strong inflammatory response. Later, the fibersenlarge, and edema, nuclear proliferation, and intestinal inflammation ensue,and fibrosis. Early symptoms of this stage are swelling（腫) of the eyelids and facial edema.Following this, muscle swelling, tenderness, pain on movement, and feverusually develop. Within the first two weeks of severe systemic disease,allergic phenomena such as edema, pneumonitis(肺炎), and pleural transudate（胸腔積液)may occur. Serious complications, including myocarditis（心肌炎), and meningoencephalitis（腦膜炎), occur most often in the thirdto ninth week of the disease.
Encystation of the larvae and tissue repair The formation of cyst result inthe stimulation of larvae and tissue reparation. With encystation, theinflammation disappear gradually, the clinical manifestation become light, butthe muscular pain can still last for months.
DIAGNOSIS
Diagnosis of Trichinosis depends on acombination of a) clinicalmanifestations with a history of ingesting meat that may contain larvae; b) immunodiagnosis; c) muscle biopsy.
Parasitic diagnosis The definitive diagnosis ismade by demonstration of free or encapsulated(囊內(nèi)) Trichinella larvae in the skeletal muscles obtained either inbiopsy or at autopsy. Muscle biopsy may be positive as early as the second weekof infection but is often not required. A small amount of muscle is excisedunder local anesthesia from a tender, painful, swollen muscle; a portion issent for routine pathologic examination; and small amount is crushed betweenglass slides and examined directly under a scanning or low power objective formotile larvae.
Immunodiagnosis a) Interdermal test (IDT) forscreening in population; b) Detecting for antibodies such as COP and ELISA etc.
EPIDEMIOLOGY
Human and animal infections of T.spiralis is worldwide distribution.In China,15 provinces have reported the infections individuals or patients. In Yunantrichinosis is the most serious zoonosis.
Three types of transmission cycle are seenin nature:
Pig-to-pig cycle This occurs in humanpopulation due to their habit of feeding garbages to pigs. Pigs fed withTrichinella scrap, pig meat or carcase of animals suffer from infection.
Rat-to-rat cycle This occurs betweenrats/mouse and is not dependent upon the presence or absence of infection inpigs.
Pig-to-rat cycle This plays an important rolein keep the transmission of infection.
It was reported that the prevalence of theinfection in pigs was 50.2% in some endemic areas of Henan province. Eating or ingesting raw porkwith larva cyst is major route to infection.
The cyst have stronger resistance to lowtemperature, freezing at -15℃ for 20 dayscan destroy the parasites in the pork. Cyst can be killed at 70℃,so eating non-properly processed meat products is the way to require infection.
PREVENTION AND CONTROL
Deep freezing at -15℃for 20 days or -30℃ for 6 daysand thorough cooking at 70℃or abovekills the larvae in the pork. Smoking, curing or drying of meet are notdependable medthods for killing the larvae.
Regular inspection of meat, avoidance ofeating raw or undercooked pork and meat of other wild animals; and avoidance offeeding raw garbage to pigs will prevent transmission of infection to man.
Treatment of the immature worms in thesmall intestine is usually successful and will abort or markedly inhibitsystemic disease, so treatment of the intestinal phase in all cases up to sixweeks after infection is advisable. Albendazole(丙硫咪唑) is the effective drug for trichinellosis. Mebendazole（甲苯咪唑)is also recommended, it isbelieve to kill both adult worms and larvae.
Angiostrongylus cantomensis(廣州管圓線蟲(chóng))
when the third-stage larva enter body by eating raw snail-meats ortransport hosts’ meats, it invade into central nervous system frequently.Common symptoms of Angiostrogyliasis are meningoencephalitis with eosinophilia,including acute headacde, nausea，vomiting and fever. Serious cases may present paralysis(癱瘓), drowsiness(嗜睡)，coma(昏迷) or death.The disease is found in tropic or subtropic areas including China, Thailand,Japan,and Vietnam etc. In Taiwan of China, it reported more 300 cases ofAngiostrogyliasis . 2 cases was diagnosed in Guangdong. Up to now, there are any specificdrugs for the disease.
Fig Ⅵ-Ⅱ-1 Life cycleof Angiostrongylus cantomensis
SectionVII MEDICAL ARTHROPOD(醫(yī)學(xué)節(jié)肢動(dòng)物)
I INTRODUCTION
Arthropods are as intimately associated with humans’ welfare as anyother animals. The economic importance of this group to agriculture, in termsof both beneficial and destructive effects, can hardly be overemphasized. Inaddition, many species have a direct relationship to human health andwell-being. The majority of arthropods function indirectly in human diseases,which they transmit but do not produce; some species are true parasites,whereas others may inflict direct injury by their bites, stings, or otheractivities. Some species are both parasites and vectors of disease. Thesearthropods related with human health are named “Medical arthropod(醫(yī)學(xué)節(jié)肢動(dòng)物)”.
Medical arthropodology (醫(yī)學(xué)節(jié)肢動(dòng)物學(xué))is a science that study themorphology, taxonomy, cycle life, zoology, geographic distribution of medicalarthropodology, and the relationship of medical arthropods with thetransmission of the disease , as well as the measures for medical arthropodscontrol.
PHYLOGENY, MORPHOLOGY, MOLTING, ANDDEVELOPMENT
The organisms in the phylum Arthropodabelong to diverse group, but they have some features in CLASSIFICATION
Medical arthropod belong to Class Crustacea（甲殼綱)， Diplopoda（倍足綱), Chilopoda（唇足綱), Arachnida（蛛形綱), and Insecta（昆蟲(chóng)綱). Among them, most medicalarthropod is from Class insecta and archnida.
Insecta: mosquito（蚊), fly（蠅), sandfly（白蛉), flea（蚤), louse（虱), cockroach（蟑螂), etc.
Archnida: tick（蜱), mite（螨), spider（蜘蛛), etc
Crustacea: crab（蟹), shrimp（蝦), etc.
Chilopoda: centipede（蜈蚣).
Diplopoda: millipede（馬陸).
HARM FOR HUMAN HEALTH
Medical arthropod can cause harm to humanby direct or indirect ways, such as bites, stings, defensive secretions or asvectors of disease.
Direct harms
1) Harassment and sucking blood(騷擾 and 吸血)
2) Allergy and toxicosis
3) Invading tissue Some larva of fliescan parasitize in the skin or the cavity , and cause myiasis(蠅蛆病). Itch mite can invade thesubcutaneous and cause scabies(疥螨).
Indirect harms Aethropods are of great importanceas vectors of disease-producing agents to humans and other animals. Diseasetransmission can be accomplished in two general ways. It may be mechanical,which means that the arthropod carries an infectious organism from one personor object to the next without serving as a host for the development ormultiplication of this organism. Transmission many also be biological, in whichcase the infectious organism develops or multiplies within the arthropod hostand is only then transmitted to the vertebrate host.
1) Mechanical transmission( 機(jī)械性傳播)
2) Biological transmission(生物性傳播)
ARTHROPOD AS A VECTOR
II CLASS ARACHNID(蛛形綱)
SCAB MITE(疥螨)
The Astigmata includes both parasitic andfree-living mites. Scab mite, Sarcoptes scabiei parasitize on humans andmammalian.. There is a single species in the genus with a number of varietiesnamed for the hosts on which they occur. S.scabiei var. humani(人疥螨) is on humans, which can causesarcoptic mange or scabies（疥瘡) and S.scabiei var. suis is on swine and so on. There is somecross-transmission possible with many varieties, but usually the ability of themites to survive and reproduce on an abnormal host is limited.
Morphology These are tiny mitesand disc-shapped, which are barely visible with the naked eye. All stages havestubby(粗短的) legs,some of which terminate in long setae（剛毛). The first two pairs of legs have roundish structwww.med126.comures calledambulacra(吸墊). In femalethe posterior two pairs of legs lack ambulacra. The female are 0.3-0.5 mm long by 0.25-0.4 mm wide, and the male are 0.2-0.3 mm long by 0.15-0.2 mm wide.
Life cycle The pattern ofdevelopment in Sarcoptes is as follows:
Egg-> larva-> protonymph (前若蟲(chóng))->tritonymph（后若蟲(chóng)) ->adult
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Fig Ⅶ-Ⅱ-10 Thedevelopment stages of SCAB MITE
Transmission from one host to the next takeplace through close contact or contamination of the environment, and any of thestages is capable of establishing an infection. Entrance into the skin isaccomplished by the mite secreting saliva onto the unbroken skin; the cells ofthe skin are lysed and the mite then eats it way into and burrows along underthe keratinized(角質(zhì)層) layers ofthe skin. The female burrows into the skin and lays eggs in a sinuous Tunnel(隧道), which she forms as sheoviposits. The eggs hatch in 3 to 5 days releasing the larval stage. The larvastill live in the tunnel or enter a new tunnel, and molts to the protonymph andthe tritonymph stage. The larvae have 3 pairs of legs and nymphs have 4 pairsof legs. The tritonymph lasts from 3 to 4 days, and then molts to reach theadult.
The female lays from one to four eggs aday, and lives about 5-6 weeks; a female lays from 40 to 50 eggs in lifetime.The male die after mating with female.
Pathogenesis The female mite selectsplaces on the body where the skin is thin and wrinkled, between fingers,wrists, elbows, feet, penis, scrotum, buttocks and axillae. The mite can causemore severe skin reactions, such as itching and allergic reactions. Theirritation and hypersensitivity seen to result from excretions, which thefemale deposit in the skin as they burrow and oviposit. Secondary bacterialinfections may also occur, probably as a result of scratching..
In young children whose skin is soft andtender, they may be found burrowing on the face and other parts of thebody.
Diagnosis Determining whether a personhas been invaded by the mites is based on the following:
Clinical signs and symptoms;
Finding the mites in the skin.
Sinuous tracks in the skin, inflammation,itching are all indicators of scab mites. Later in the infection, crustypatches are seen. The crux（結(jié)痂) of the matter is finding the mites in the skin, but it is necessaryto scrape the skin somewhat nevertheless.
Scraping are examined under a compoundmicroscope for mites, parts of mites, eggs and fecal pellets.
Control The transmission ofthe disease is accomplished by direct contact with the infected person or withtheir clothing or bedding. For scabies control, the acaricides can be applied to skin after a hot, soapy bath.All clothing and bedding should also be laundered.
The acaricides include 10% Brimstoneointment(硫磺軟膏) etc.
DEMODICIDAE MITE(蠕形螨)
Demodicidae mite belong to FamilyDemodecidae. Demodex spp are all parasites of mammals. They cause a diseaseusually called demodectic mange or demodecosis（蠕螨病). Members of the genus have a high degree of both host and sitespecificity. Human have two species, D. folliculorum（毛囊蠕形螨), which lives in hairfollicles, and D. brevis（皮脂蠕形螨), which is found in sebaceous glands（皮脂腺).
Morphology Demodex spp. are elongateand have four pairs of stubby legs. The mouthparts are not apparent and thehysterosoma(末體) is quitelong.
Fig Ⅶ-Ⅱ-11 Adult of Demodicidaemite
Life cycle The mites live in hairfollicles, sebaceous gland, and sweat gland depending on the species. Thefollicles or glands may become packed with mites. Transmission between hosts isby close bodily contact. The pattern of development is as follows:
Egg-> larva-> protonymph (前若蟲(chóng))->nymph（若蟲(chóng)) ->adult
The life cycle probably require about ahalf month. The female live more than 4 months, and the male will die aftermating.
Diagnosis and control The presence of the mite canbe determined by gently squeezing（擠) the skin and looking for the mite in the exudates（滲出物). They are seen mostly on theface in oily areas, such as around the nose, or in the eyebrows and eyelasheswhich may be plucked and examined under a microscope.
The acaricides include 10% Brimstoneointment(硫磺軟膏) etc。
