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Ascaris lumbricoides

Disease. Ascariasis, ascaris infection, roundworm infection

Geographical Distribution. It is cosmopolitan, having a world-wide distribution, beingspecially prevalent in the tropics, such as China, India and Pacific Islands. It occurs in

persons with unhygienic habits

Habitat. The adult worm lives in the lumen of the small intestine of man and maintainsits position by its muscle tone.

Morphology. The white or pink worm is identified by: (1) large size, male 150-200 x 2-4

mm and females 200 -350 x 4 -6 mm; (2) smooth finely striated cuticle; (3) conical

anterior and posterior extremities; (4) ventrally curved papillated posterior extremity of male with 2 spicules; (5) terminal mouth with 3 oval lips with sensory papillae; and (6)

paired reproductive organs in posterior two thirds of female and single long tortuous

tubule in male.

The eggs measure 45-70 x 35-50 µ. There is an outer, coarsely mammilated, albuminouscovering which serves as an auxiliary barrier to permeability, but may be absent. The egg

proper has a thick, transparent, hyaline shell with a relatively thick outer layer that acts asa supporting structure: and a delicate vitelline, lipoidal, inner membrane that is highly

impermeable. At oviposition the shell contains an ovoid mass of unsegmented protoplasm

densely impregnated with lecithin granules. The typical infertile eggs 88-94 x 39-44 µ arelonger and narrower than fertile eggs, have a thinner shell with an irregular coating of

albumen and are completely filled with an amorphous mass of protoplasm, with refractile

granules. Bizarre shaped eggs without albuminous coating or with abnormally extensive

and irregular coating are also found. The infertile eggs are difficult to identify and may bemissed by the unwary and untutored. They are found not only in the absence of males but

in about two fifths of all infections, since repeated copulations are necessary for thecontinuous production of fertile eggs.

Life cycle. The worm passes its life cycle in one host and no intermediate host is

required. Continuance of the species is maintained by transference from one individual to

another. Man is the only known definitive host of A. lumbricoides. The various stages inthe life cycle are described below:

STAGE 1. Eggs in Faeces. Fertilised eggs containing the unsegmented ovum are

passed with the faeces. They are not infective to man when freshly passed.

STAGE 2. Development in Soil. A rhabditiform larva is developed from the unsegmentedovum within the egg shell in 10 to 40 days’ time, depending on the atmospheric

temperature and humidity. This takes place in the soil (that is outside the human host).

The ripe egg containing the coiled-up embryo is infective to man. Before hatching, thelarva undergoes a moulting.

STAGE 3. Infection by Ingestion and Liberation of Larvae. When ingested with food,

drink or raw vegetables, the embryonated eggs pass down to the duadenum where thedigestive juices weaken the egg-shell and stimulate the enclosed larvae into activity.

Splitting of egg-shell occurs and the rhabditiform larvae measuring 0.25 mm. in length by

14 µ in breadth are liberated in the upper part of the small intestine.



STAGE 4. Migration through the Lungs. The larvae liberated in the small intestine do not

directly develop into mature worms. The newly hatched larvae burrow their way through

the mucous membrane of the small intestine and are carried by the portal circulation tothe liver; here they live for a period of 3 to 4 days. Finally they pass out of the liver and

via right heart enter the pulmonary circulation. While in the lungs they grow much bigger

and increase in length from 0.2 mm to 2 mm. and moult twice (first, on the fifth or sixthday and the second, after the tenth day). Breaking through the capillary wall they reach

the lung alveoli. The time taken for such migration is on an average 10 to 15 days.

STAGE 5. Re-entry into the Stomach and the Small Intestine. From the lung alveoli thelarvae crawl up the bronchi and trachea, and aided by the current caused by the ciliated

epithelium of the respiratory tract, they are propelled into the larynx and pharynx and are

once more swallowed. The larvae pass down the oesophagus to the stomach and localise

in the upper part of the small intestine, their normal abode. Another moulting occurs between the twenty-fifth and the twenty-ninth day of infection.

Stage 6. Sexual Maturity and Egg Liberation. The larvae on reaching their habitat grow

into adult worms and become sexually mature in about 6 to 10 weeks’time. The gravid

females begin to discharge eggs in the stool within about two months from the time of infection. The cycle is again repeated.

Note: Four moultings of the larva occur- one outside while within the egg-shell, two inthe lungs and one in the intestine.

MODE OF INFECTION. Infection is effected by swallowing ripe Ascaris eggs

(embryonated eggs) with raw vegetables cultivated on a soil fertilised by infected humanexcreta. Water-supplies may be contaminated and infection may occur by drinking such

water. Where soil-pollution is common, the eggs may directly be conveyed to he mouth

by dirty fingers.

Infection may also occur by inhalation of desiccated eggs in the dust reaching the pharynx and swallowed. The eggs, instead of being swallowed, may hatch on moist

mucous surface of the upper air passage and the larvae may directly penetrate into the

blood stream.It may be remarked that porcine infection does not play any part in the etiology and

epidemiology of human ascariasis. The infective-stages are invariably obtained from

human sources. Infecting Agent— Embryonated egg.

Portal of Entry---Alimentary canal.

Migration of Larvae --- Through lungs.

Site of Location---- Small intestine Pathologenicity and Clinical features. Infection of A. lumbricoides in man is known as

ascriasis, the symptoms attributed to Ascaris infection may be divided into two groups:

(a) those produced by the migrating larvae and (b) those produced by the adult worms.



SYMPTOMS DUE TO THE MIGRATING LARVAE

Larvae in the Lungs: Ascaris Pneumonia ( Loeffler’s Syndrome). In heavy infectionstypical symptoms of pneumonia such as fever, cough and dyspnoea may appear. Sputum

which is often blood-tinged may contain Ascaris larvae. Urticarial rash and eosinophilia

(20 per cent.) are seen in such cases. Larvae in General Circulation. If the Ascaris larvae pass beyond the pulmonary

capillaries and reach the general circulation, they are filtered out to various organs where

they may set up unusual clinical symptoms. Disturbances have been reported due to their presence in the brain, spinal cord, heart and kidneys.

SYMPTOMS DUE TO THE ADULT WORLMS

Incubation Period. In man it takes 60 to 75 days from the time of exposure to infection,

for the mature female to lay eggs and that is the period when the symptoms ate

manifested.

Pathogenesis. As the worm inhabits the upper part of the small intestine, the symptoms

are therefore mostly related to the gastro-intestinal tract. The adult worm may produce its pahogenic effects in the following ways:

(1) :SPOLIATIVE ACTION: By robbing the host of its nutrition (protein and

vitamin content of the worm is high). This effect is readily observed in hyperinfectedchildren and may contribute to protein-calorie malnutrition.

(2) “TOXIC” ACTION: the body fluid of Ascaris when absorbed is toxic and

may give rise to typhoid-like fever; also responsible for various allergic manifestations

such as urticaria, oedema of the face, conjunctivitis and irritation of the upper respiratorytract.

(3) MECHANICAL EFFECTS: (i) The presence of A. lumbricoides has led to the

occurrence of intussusception; (ii) it may penetrate through the ulcers of the alimentarycanal; (iii) a large number of Ascaris has been known to produce intestinal obstruction.

Ectopic ascariasis. The worms frequently migrate and may enter the stomach

hand may be vomited out or may pass up through the oesophagus at night, coming outthrough the mouth or nose. Thus during migration, Ascaris worms may accidentally enter

into the respiratory passage causing suffocation b blocking the rima glottidis or may even

enter into a bronchus.

Wandering Ascaris may enter the lumen of an appendix, causing appendicitis.Obstructive jaundice and acute haemorrhagic pancreatitis have been known to occur

when the worm has entered into the biliary passage. At times it penetrates high up in the

liver causing one or more abscesses.

Diagnosis. The clinical symptoms of intestinal ascariasis area indistinguishable from

those of other intestinal helminthic infections. Ascaris pneumonitis, although the

symptoms are fairly characteristic, is usually mistaken for an atypical pneumonia.Diagnosis is made by finding the fertile and/or infertile eggs in the feces. The numerous

fertile eggs are detected in the direct coverglass mount. If direct examination is negative,

concenration technics may be employed. Infertile eggs are more easily missed by the

examiner than any other nematode eggs and virgin ascariasis is often overlooked. Egg



production is fairly constant and egg-counting method give a fairly reliable index of the

number of worms. The adult worm may be detected radiologically. This is obviously the

only way an infection with only immature and male worms may be detected.

Treatment. For ascariasis the drug of choice is peperazine salts. Other drugs: pyrantel

pamoate, thiabendazole and mebendazole.

Prophylaxis. The measures should consist of (i) proper disposal of human faeces, (ii)treatment of parasitised individuals and (iii) education of children in schools on sanitary

laws and hygiene.



Paragonimus westermani

Common Names: The Oriental lung fluke,

the lung distomeGeographical Distribution. Japan, China, Korea, Vietnam, Thailand, Cambodia, India,Micronesia, Irian Jaya, Papua New Guinea, and the Phillippines. Also reported from

some parts of Africa and South America.

Habitate. Adult worms live in the respiratory tract (lungs) of man

Morphology. Adult worm. It is thick, flashy and egg-shaped. Its anterior end is slightly

broader than the posterior end. It measures 8 to 12 mm. in length by 4 to 6 mm. in

breadth and 3 to 5 mm. in thickness. The ventral sucker is situated near about the middle

of the body. The excretory vesicle is large and extends from the posterior extremity to the

anterior region, dividing the body into two equal halves. The two blind intestinal caecaare unbranched and extend to the caudal region. The genital apparatus follows the same

general pattern of trematodes.

Life span of the adult worm is about 6 to 7 years.

Eggs. These are golden brown in colour, oval in shape and are provided with

flattened opercula. They measure 80 µ 55 µ and each egg contains an unsegmented ovumsurrounded by yolk cells.

Life Cycle. Infection begins by ingesting the metacercariae. They excyst in the small

intestine, penetrate into the abdominal cavity, and within several days, develop toimmature flukes. They then migrate to the lungs by penetrating the diaphragm, and

mature to reproductive adults within 8-12 weeks. Worms also locate to aberrant sites,

including brain, liver, intestines muscle, skin and testes. In these sites, passage of eggs tothe external environment is impossible.

The pair of adults usually cross-fertilize each other. Both diploid and triploid form

produces eggs via parthenogenesis. Egg production begins about 30 days after infection

of the metacercariae. Eggs pass fertilized, but unembrionated into the surrounding tissue.Eventually, they reach the bronchioles, and are included in the sputum. Which also

contains blood and debris from the necrotic lesions created by the adults. The number of

eggs produced by each worm is unknown. Because some of the sputum is swallowed,eggs can be recovered from feces. The eggs must reach fresh water to embryonate. The

miracidium develops over a 3 week period, after which it hatches and seeks out its

intermediate host snail (e.g. Melania sp., Semisulcospira sp., and Thiara sp.). They

develop through the sporocyst and redia stages into cercariae, which then exit from thesnail and encyst upon and within crustacean intermediate host. In the case of the crab, the

metacercacriae infect all organs.

Pathogenicity and Clinical Features. Infection with P. westermani is known as paragonimiasis.

Mode of infection. Eating of raw or improperly cooked flesh of an infected crab or

crayfish. Infecting Agent - Metacercaria or adolescaria inside a cyst.



Portal of entry- Digestive tract.

Site of Localisation- Lungs.

The symptoms of paragonimiasis are chronic cough with recurring attacks of haemoptysis, simulalting a case of bronchiectasis or pulmonary tuberculosis.

Although the lung is the normal site of localisation for the young parasite, it can enter

any organ of the body, such as liver, intestine, peritoneum and other organs. The clinicalmanifestations in these cases depend on the organs involved. In case of abdominal

organs, the symptoms include pain in the abdomen, diarrhoea and enlargement of the

liver. In cerebral infection, Jacksonian type of epilepsy and other symptoms characteristicof brain tumour develop and may even terminate fatally. In generalised paragonimiasis,

there is fever, generalised lymphadenitis and cutaneus ulceration.

Diagnosis. This is determined by the presence of the characteristic eggs in the sputum

when examined under the microscope. Eggs have also been detected in the stool. Indirectevidence of infection is obtained by serological tests, such as ELISA and Western blot.

There is also a simple and rapid intradermal test, performed by injecting diluted

Paragonimus antigen into the skin. Using this procedure, over 2 million people have been

tested in China to date, with an over all positivity rate of 20%. Both the serologic andintradermal assays indicate either current or past exposure to the infection.

Differential diagnosis. Pulmonary paragonimiasis must be distinguished from chronic bronchiectasis, and lung abscess due to other causes, and tuberculosis. Cerebral

paragonimiasis must be distinguished from the more likely b

brain tumors, and lesions caused by other helminths.

Treatment. The drug of choice against Paragonimus westermani is praziquantel. The

drug is also effective against extra-pulmonary forms. An alternative drug, triclabendazole

is also effective.

Prophylaxys. The measures include (1) disinfection of the sputum and faeces,(2)eradication of molluscan host and (3) avoidance of the consumption of raw, freshly salted

or inadequately cooked crabs and crayfish as food.



Pneumocystis (carinii) jiroveciPneumonia

Background

Pneumocystis jiroveci , previously known as Pneumocystis carinii, is the organismresponsible for Pneumocystis carinii pneumonia (PCP); the most commonopportunistic infection in HIV-infected patients. As our understanding of thePneumocystis genus has grown, the name was changed to specifyPneumocystis, which is isolated in humans. The abbreviation PCP is still used todesignate Pneumocystis pneumonia. Pneumocystis is a genus of unicellular fungi found in the respiratory tracts of many mammals and humans. Distinctgenomic variability exists between host-specific members of the genus. Theorganism was first described in 1909 by Chagas then a few years later by

Delanöes who ultimately named the organism in honor of Dr Carini after isolatingit from infected rats. Years later, Dr Otto Jirovec and his group isolated theorganism from humans, and it is after him that the organism responsible for PCPpneumonia was renamed.

Pneumocystis first came to attention when it was found to cause interstitialpneumonia in Central and Eastern Europe during World War II in severelymalnourished and premature infants. Prior to the 1980s, fewer than 100 cases of PCP occurred per year in the United States, occurring in immunosuppressedpatients such as cancer patients treated with chemotherapy and solid organtransplant recipients on immunosuppressive agents. In 1981, the Centers for

Disease Control and Prevention (CDC) reported the occurrence of PCP in 5previously healthy homosexual males residing in the Los Angeles area.Pneumocystis jiroveci is now one of several organisms known to cause life-threatening opportunistic infections in patients with advanced HIV infectionworldwide.

Microbiology

The taxonomic classification of the Pneumocystis genus was debated for sometime. It was initially mistaken as a trypanosome then later as a protozoan. In the1980s, biochemical analysis of the nucleic acid composition of Pneumocystis

rRNA and mitochondrial DNA identified the organism as a unicellular fungusrather than a protozoa. Subsequent genomic sequence analysis of multiplegenes including elongation factor 3, a component of fungi protein synthesis notfound in protozoa, further supported this notion. The organism is found in 3distinct morphologic stages. The trophozoite or trophic form, where it often existsin clusters; the sporozoite, which is a precystic form; and finally, the cyst, whichcontains several intracystic bodies also known as spores.



Pathophysiology

Pneumocystis is commonly found in the lungs of healthy individuals. Mostchildren are believed to have been exposed to the organism by age 3 or 4 years,and its occurrence is worldwide.

Animal studies have suggested that Pneumocystis is communicable withairborne transmission reported. Human evidence of this is provided by molecular analysis of Pneumocystis isolates obtained from groups of patients involved inhospital outbreaks. Further evidence of human transmission is found in cases of recurrent pneumonia where the genotype of Pneumocystis in the same personwas different in prior episodes.

Disease occurs when defects exist in both cellular immunity and humoralimmunity. Once inhaled, the trophic form of the organism attaches to the alveoli.Multiple host immune defects allow for uncontrolled replication of the organism

and development of illness including the following:

• Activated alveolar macrophages without CD4+ cells are unable to

eradicate the organism• Increased alveolar-capillary permeability documented on electron

microscopy• Physiologic changes that occur include the following:

o Hypoxemia with an increased alveolar-arterial oxygen gradient

o Respiratory alkalosiso Impaired diffusing capacity

o Changes in total lung capacity, vital capacity

Frequency

United States

Prior to the widespread use of PCP prophylaxis, the frequency of infection in lungtransplant patients alone was as high as 88%. Now with routine use of prophylaxis, PCP is very rare in solid organ transplant patients and hassignificantly decreased in HIV patients.

• Prior to highly active antiretroviral therapy (HAART), PCP occurred in 70-

80% of HIV-infected patients.• The frequency of PCP is decreasing with the use of PCP prophylaxis and

HAART.• PCP is still the most common opportunistic infection in HIV patients.

• HIV patients are more prone to recurrence than patients without HIV.



International

The prevalence of PCP was once thought to be much lower in developingregions of the world, but studies have shown that the lower incidence reported islikely a failure to accurately diagnose the condition. Accurate diagnosis requires

access to modern medical care not available worldwide. Now, the frequency of documented infection is increasing in Africa, with Pneumocystis found in up to80% of HIV-infected infants with pneumonia.

Mortality/Morbidity

• In HIV patientso Mortality used to range from 20-40%, depending upon disease

severity at presentation. Now, mortality rates of 10-20% arereported.

o PCP is still a major cause of death in AIDS patients in the United

States.• Non-HIV patients

o The outcome is worse in non-HIV patients without a significant

change in 20 years.o Mortality rates of 30-50% have been documented in several large

studies.o Higher incidence of mortality is likely a result of a delay in diagnosis

and initiation of appropriate treatment.

History

The symptoms of PCP are very nonspecific. HIV-infected patients tend to have amore subacute indolent course and tend to present much later, often after several weeks of symptoms, when compared with other immunocompromisedpatients. Symptoms include the following:

• Progressive exertional dyspnea (95%)• Fever (>80%)

• Nonproductive cough (95%)

• Chest discomfort• Weight loss

• Chills

• Hemoptysis (rare)



Physical

Like the history, the physical examination findings of PCP are very nonspecific

and include the following:

• Tachypnea

• Fever

• Tachycardia

• Pulmonary examination may reveal mild crackles and rhonchi but may be

normal in up to half of patients.• Additional findings in children with severe disease

•

o Cyanosiso Nasal flaring

o Intercostal retractions• Extrapulmonary manifestations: While extrapulmonary manifestations are

rare with Pneumocystis, they may be present in patients receivingaerosolized pentamidine for prophylaxis or in patients with advanced HIVinfection who are not taking any prophylaxis. They may also occur in theabsence of lung involvement. Pneumocystis may present in almost anyorgan system with the most well-documented findings, as follows:

•

o Hepatomegaly

o Skin lesions

o Bone marrow (may have necrosis with resultant pancytopenia)

o Lymphadenopathyo Eyes (may have retinal cotton-wool spots)

o Thyroid (may present as a rapidly enlarging thyroid mass)

o GI tract

Causes

P jiroveci causes PCP in the following patients:

• HIV patients when the CD4+ cells fall below 200/µL and not taking PCP

prophylaxis; findings of other opportunistic infections such as oral thrush inan HIV patient increases the risk of PCP regardless of CD4+ count.

• In other patients with primary immune deficiencies including

hypogammaglobulinemia and severe combined immunodeficiency (SCID).• In patients on long-term immunosuppressive regimens for connective

tissue disorders, vasculitides, and solid organ (eg, heart, lung, liver kidney) transplant recipients



• Patients with hematologic and nonhematologic malignancies including

solid tumors and lymphomas• Patients with severe malnutrition

DIFFERENTIALS

Acute Respiratory Distress SyndromeCytomegalovirusLymphocytic Interstitial PneumoniaMycobacterium Avium-IntracellulareMycoplasma InfectionsNocardiosisPneumonia, BacterialPneumonia, Community-AcquiredPneumonia, Fungal

Pneumonia, ViralPulmonary EmbolismTuberculosis

Medical Care

Although officially classified as a fungus, PCP does not respond to antifungaltreatment. Although a histopathologic demonstration of the organism is required

for a definitive diagnosis, treatment should not be delayed. The organism persistsin its host for anywhere from days to even weeks after therapy is started,allowing time for the appropriate workup to still be completed.

• Treatment depends upon classification of degree of illness at the time of

diagnosis (see Medication below).• Treatment is based upon the alveolar-arterial gradient, which may be mild

(<35 mm Hg), moderate/severe (35-45 mm Hg), or severe (>45 mm Hg).• Severe disease is also diagnosed by a room air pO2 of less than 70 mm

Hg.

Drug: Antibiotic

Primary recommended treatment for mild, moderate, or severe disease. TMP-SMX has been shown to be as effective as intravenous pentamidine and moreeffective than other alternative treatment regimens. The parenteral route may beconsidered in patients who present seriously ill or in those with gastrointestinalside effects. TMP-SMX is the preferred initial therapy during pregnancyaccording to consensus guidelines. The patient's neonatologist should be

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informed if the medication is used near delivery because of potential for hyperbilirubinemia and kernicterus.

Complications

• Hypoxemia and respiratory failure

•

o A pathophysiologic process similar to ARDS occurs in patients with

severe PCP.o These patients may need intubation and have a significantly worse

prognosis.

Prognosis

• The prognosis is worse in patients who present with concurrent pulmonarydisease, in patients who develop a pneumothorax, and in patientsrequiring mechanical ventilation.

• Other factors affecting prognosis include a delay in diagnosis leading to

delayed treatment

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