12 Aug 2018


A wart is a viral infection of the surface layers of the skin. The incubation period varies from a few weeks to several months. Warts can be spread by direct or indirect contact with a wart to damaged skin.


A corn is a small, hardened area of skin which often looks yellow compared to the surrounding skin. It is typically round or corn-shaped, pointing down into the skin. Corns most often form on the feet and sometimes on the hands and are caused by constant or repeated friction or pressure.


A callus is rough, thickened skin spread over a wide area. Like a corn, it caused by constant or repeated friction or pressure, but unlike corns, calluses are flat and have normal skin markings.

07 Jul 2018

INTRODUCTION: Mental Retardation

Mental retardation (MR), defined as a failure to develop a sufficient cognitive and adaptive level. It is one of most common human disease. Also, 1-3 % of the human population has an IQ below 70. Recent research has discovered that MR is related to the presence of certain mineral elements in the body above-normal levels, especially cadmium and lead (Mike et al. 1983). It has been estimated that half of all cases are due to environmental factors, that include prenatal exposure of the fetus to toxic substances, environmental contaminants, infections, radiations, illness of mother (eg exposure to rubella, Cytomegalovirus) and malnutrition etc. (Birgitta et al. 2003). The prevalence of Intellectual disability (ID) also referred to as mental retardation is between 1% and 3% (Roeleveld et al. 1997; and Wen 2002). And ID is present in every social class and culture (Leonard and Wen 2002). Also, there are approximately 30% more males with MR are diagnosed than females (American Psychiatric Association 2000; Miclaren and Bryson 1987). Alzheimer’s disease (AD) is a mental retardation mostly caused by cadmium. Also, blood cadmium concentration in Alzheimer’s disease and non-demented subjects were studied. Smokers had higher cadmium level than non-smokers.

Alzheimer’s disease: A case study.

A 59 years old university teacher with Alzheimer’s disease visited our clinic and treated for five weeks from November 9 to December 15, 1995. She was suffered from memory loss and had been getting professional terms, and concepts forced her to resign at the university. She was admitted to the clinic. In day to day matters she was forgetting to switch off electronic devices and other appliances, and continuously became lost even in her own neighborhood. She suffered an acute onset of the disease and had been ill for 13 months. His history showed that first bouts of amnesia lasted three to four hours. Also, an increase in dementia and memory loss was registered. Her blood pressure rose to 150/90 mm. Also, her brother had suffered similar memory loss and died at age 57, also her mother suffered from dementia, beginning at age 52 and died at age 56. So it was discovered that this predisposition was based on genetics and not on gender.


Routine examination of internal organs showed no pathology. No local pathology in routine neurological tests.

Mental State

Critical behavior was preserved. The acute memory loss, concerning life events, such as children and even she was unable to recall her maiden name. Also, she had difficulty with the execution of simple arithmetic operations and her logical thinking diminished.

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CT scan is done, which showed the atrophy of the cortex and widening of subarachnoidal spaces and also brain ventricles. Roentgenoscopy showed some reduction of blood flow in all areas. Slowing of the main cortex rhythm observed with EEG. Also, the blood test showed slightly elevated blood cholesterol.


The patient was treated with cerebrum composition, one ampule injection three times a week. Cerebrum composition is a complex homeopathic formula produced in ampules of 2.2 ml. Also, each ampule contains in its formula as ingredients.


1st and 2nd week: No change.

3rd week: some improvements, and she became more physically active, but no changes in her state of memory.

4th week: the ability to perform routine tasks improved. She was able to retell articles and her ability to perform arithmetic operations was improved.

5th week: there were improvements in her abilities including abstract logical thinking and her mood.


Strong metal cadmium appears in earth crust that spread in the environment by two processes as like human activities and by a natural process such as waste incineration, the use of phosphate fertilizers fossil fuel burning smelting procedures (Agency for Toxic Substances and Disease Registry 2008). Cadmium is found in soil, plant, animal tissues, air, and water (Friberg, et al. 1979). Cadmium is a heavy metal, has no useful natural role (WHO, 1992; NRC, 2005), and may be extremely toxic when presented into the body through absorption.

Cadmium sources:

Food Sources:

Food sources of cadmium are rice and wheat grown in the soil which is contaminated by different fertilizers such as phosphate and by wastewater.

Different fish also contains a large quantity of cadmium in their tissues such as tuna, haddock, and codfish. Oyster also contain Cd in great amount but it also has zinc which prevents it from toxicity produced by Cd.

During the processing of food, zinc is removed, which protects food from toxic effects caused by cadmium so Cd remains in food which is harmful.

Refined & processed food:

Refined foods have such elements such as zinc and calcium which provide protection but in some cases, these elements are removed so Cd remained in food which easily absorbed in food.

We can use Cd for plating purpose in the plants of food processing. Different processed foods such as meat, grains, carbonated drinks, coffee are a common source of cadmium that causes toxic effects in our body.

Nowadays we mostly use white rice and flour which are deficient in vitamins and minerals, this deficiency causes to enhance Cd level.

Another source of Cd toxicity is the usage of carbohydrates in large amount. Because it reduces the zinc level.

Drinking Water:

Cd is used in many industries so when industrial wastes are disposed of cadmium enters in our drinking water. In hard water, there is a large amount of calcium which protects from toxicity but soft water having low calcium contents is more harmful. Plastic and galvanized pipes are also a source of cadmium.

Batteries, Semiconductors, Electroplating, Polishes:

Information industries of different electrical goods, cadmium is used.labours of these industries have a high risk of toxicity. Dentists also use Cd in making artificial teeth and in their polishing process.

The smoke of cigarettes:

Cigarettes have high cadmium contents so when smoke is inhaled it absorbed in our lungs. One packet contains 2-4 micrograms Cd.

Other sources:

Cadmium is present in motor oil rubber goods, tiers in paints and plastic. Vehicles exhaust has a high level of Cd.

Congenital Cadmium Intoxication:

It was observed in rat pregnant mother after giving a continuous injection of cadmium, it enters into the brain of its fetus. Nowadays high amount of cadmium is being observed in babies and in young people, we can say that this high amount of source in babies is their mothers. This can cause severe birth defects and abnormalities such as learning disorders, hyperkinesis, and minimal brain dysfunction.

How to detect cadmium:

Blood Tests:

As we intake cadmium in different forms from various food sources, but its blood level is low so detection of it through blood test does not give us the clear result.

Challenge Tests:

To detect cadmium we use chelating agents. The urine sample is collected (24-hour sample) to detect Cd level in blood and arteries.but this test is not used in the detection of cadmium in bones, joints, and other tissues.

Detection from hair analysis:

There is a specific relation between cadmium level in hair and kidneys. If Cd concentration is high in hair its mean its level is also high in kidneys. Cd identification or detection is not done on the first test because Cd is bound with other elements and it takes time to release from this tight binding.

Cadmium metabolism:


Cadmium is highly absorbed through inhalation. Risks of cadmium toxicity in women are more than in men because metabolic rate is slower in women. Low  level of calcium, zinc, protein, and iron in body favors more absorption of cadmium in the body


Half of the total amount of cadmium inhaled, absorbed in the body is stored in liver and kidneys. Cadmium also stored in the pancreas and salivary glands. It may also store in

Joints, periosteum or bone covering, in arteries and in all other body tissues. Cadmium moves from plasma to RBCs and binds with hemoglobin and metallothionein. Cd inhalation activates the production metallothionein, it is a protein binds with Cd and zinc. Cd varies in concentration with respect to age.

In newborn, its concentration is 15-20mg and in adults less than 1mg.


Metallothionein a chelating agent performs its part in excretion of Cd. This process of excretion is done through kidneys and liver but this process is very slow.10-30 years is the half-life period of cadmium.

Cadmium metabolic effects:

Energy Production:

One of the inhibitors of cellular respiration is cadmium. As it forms a strong bond with many bio-elements so it is very harmful to the human body. These biomolecules include many enzymes of the Kreb cycle.

Zinc displacement:

Harmful effects of cadmium mostly appear in kidneys, nervous system and arteries. It is observed that many birth abnormalities are caused just due to Cd.

Cadmium binds faster with metallothionein as compared to zinc and copper, so this strong binding of Cd causes a deficiency of zinc and copper. For utilization of zinc and copper it is important that these two elements bind with metallothionein but as we know cadmium binds more fastly than these cadmium poisoning results into a low level of zinc and copper. Another feature is that,( poisoning caused by Cd) the replacement of zinc with cadmium in enzyme system results in the very critical situation because Cd can do homeostatic function. So that many enzymes of zinc can perform their functions with Cd so in this way the enzymatic action is not proper it becomes slow which finally results in impairment of enzymes which are dependent on zinc.

Renal Effects caused by Cd:

As cadmium is stored in kidneys, this storage causes the malfunctioning of renal.

When renal not performs well it strongly affects the concentration level of calcium-vitamin D phosphorus and sodium level. These low levels of elements result in different problems such as renal hypertension, proteinuria, glycosuria, and other disorders of metabolism.

Carcinogenesis and Teratogenesis:

It is observed now that calcium causes cancer. Abnormalities occurring at the birth time are usually due to low level of zinc. Mostly mice and rat are being observed suffering from these abnormalities caused by Cd.

Metabolism dysfunction due to a high level of Cd:

Metabolism dysfunction due are categorized into different types which are as follow

Nervous System:


Cd by disturbing calcium metabolism stops the release of acetylcholine.zinc stops the action of cholinesterase but cadmium enhances the action of this enzyme. Cadmium also stops the adenylate cyclase monoamine action.

Other damage caused by cadmium:

Cadmium also harmful for nerve cells and also for nerve fibers. It induces the hemorrhages in the autonomic ganglia. It can also cause Peripheral neuropathy.

Muscular-Skeletal System:

Cadmium alters the different metabolic pathways as do with zinc and calcium.

This alteration results in osteoporosis and arthritic disorders in case of protein. In the case of zinc deficiency, neuromuscular dysfunctions occurred.


Decreased strength and flexibility in arteries is mainly due to the low level of zinc. This deficiencies also caused the narrowing of arteries.

Digestive System:

Cadmium interaction with different enzymes such as zinc-dependent enzymes may result in improper digestion.

Endocrine/Metabolic System:

Zinc is necessary for growth. Growth disorders and failures may be caused by cadmium.


Disorder of Calcium and vitamin D metabolism results in deformities of teeth and dental caries.


Hyperactivity and learning disorders are caused by cadmium. Acetylcholine release is disturbed by Cd results in hyperkinetic behavior.

Metabolic Dysfunctions Associated With Cadmium Toxicity


This is linked with a deficiency of zinc and with the low level of calcium. We can say that Cd causes alcoholism because it is the main reason for zinc deficiency.

Loss of hair (Alopecia):

This phenomenon is mainly associated with zinc deficiency results due to inhalation and absorption of cadmium.


Early symptoms showing cadmium poisoning is anemia.


Proper metabolism of fats is done in the presence of zinc. But when this optimal level is disturbed.atherosclerosis occurs.


As zinc is necessary for the flexibility of arteries. But by replacement of zinc with Cd results into disorders of arteries. Due to the low level of zinc arteries have high risks to rupture and becomes less flexible. In this critical situation, the body accumulates calcium which may provide strength to the walls of arteries.

Arthritis, Osteo, and Rheumatoid:

Zinc replacement causes by Cd disturbed the protein formation. So in this way less and improper protein formation occurs resulting in pain and inflammation of joints.

Bone Repair, Inhibited:

Cadmium can replace calcium in our bones.

When any damage occurs in bone or breakage zinc is the element requires for bone repair.

Cerebral Hemorrhage:

Cerebral hemorrhage caused due to cadmium toxicity. Weakness and loss of flexibility of cerebral arteries caused by cadmium.

Liver Cirrhosis:

Liver cirrhosis is caused by low level of zinc-induced by cadmium detoxification in the liver.


The complete process of insulin from production stage to transport and usage zinc is very essential. But with the interference of Cd zinc metabolism is disturbed which leads to induce diabetes.


It is the condition in which fragile alveoli of lungs are broken and alveoli get brittle. This condition is caused when zinc is replaced by cadmium in collagen.

Enlarged Heart:

Cadmium is the most common element causing various heart disease. As it causes the reduced flexibility of arteries, in addition to this, it causes the enlargement of heart size and high blood pressure.

Fertility, Decreased:

Cadmium induces the deficiency of zinc which regulates the fertility of males. Due to this sexual potency is decreased.


Hemochromatosis is the situation of high accumulation of iron in the body tissues. This occurs when the liver fails to detoxify iron. Loss of this detoxification of iron is due to cadmium. One reason for hemochromatosis may be decreased level of calcium and copper.

Hypercholesterolemia and Hyperlipidemia:

Low level of zinc leads to increase the level of cholesterol. This increased level of cholesterol may affect the normal function of the liver.


Cadmium is one of the reasons for hypertension and high blood pressure.


Zinc deficiency may leads to hypoglycemia.

Lung Disease:

Cadmium is harmful to lungs as it inhaled with the cigarette smoke it affects the elasticity of lung tissues.

A migraine Headache:

By interfering with zinc metabolism, cadmium toxicity may allow tissue copper buildup to occur, resulting eventually in the causation of migraine headaches.


Zinc is an essential element which stabilizes the CNS and it is a neurotransmitter.

Low level of it may cause the mood disorders and this low level allow copper to accumulate in the brain. This accumulation of copper is one of the reasons for schizophrenia.

Vascular Disease – Strokes (cerebral vascular disease):

Due to the replacement of zinc with the cadmium arteries loss their flexibility and have high risks of rupturing, in this situation body covers the arteries with fatty acids or calcium which provide protection to walls of arteries. If a small part of plaque breaks, it can block the arteries causing a vascular stroke.


Alzheimer’s disease (AD) is a neurodegenerative infection that is categorized by dementia as the main medical feature of Alzheimer’s disease. Mostly affects the mature and has become one of the foremost mortal infections. Classic neurotic structures of AD contain β-amyloid protein (Aβ) confession in the brain that forms. Forgetful plates (SPs), neurofibrillary twists (NFTs) and neuronal apoptosis. Cadmium (Cd) is an injurious hint element that reasons living abnormalities and morphological of the central nervous system (CNS) mental retardation and memory loss (Wu et al. 2001). Concentrations of Cadmium and Cd/Zn are expressively higher in the hair of AD patients and blood than in vigorous people.

However, the association between Cadmium and Aβ has occasionally has been studied. Identification of three loci—on chromosomes 6p21, 10q24, 11q23—that produced helpful effects in three or more self-governing studies, in addition to the deep-rooted Alzheimer’s disease relationship with the gene encoding Apolipoprotein E (APOE) (Bertram et al., 2004). There is a noticeable damage to noradrenergic, cholinergic, and dopaminergic neurons in the AD. The decrease of turgid A deposits with trashes of monoclonal antibodies against A  that absence the Fc portion recommends a non-Fc-mediated appliance of consent.

While current proof proposes that Alzheimer’s disease is a varied disorder including numerous diverse genotypic and phenotypic expressions, Alzheimer’s disease can be categorized clinically by an advanced deficiency in mental retardation purpose throughout mid- to late-adult life with the primary symptoms naturally being sure practices of language and memory losses.

Brains from Alzheimer’s (AD) disease patients expression numerous neuropathological features, with intracellular and extracellular amyloid- (A ) peptide-containing plaques neurofibrillary masses of unusually astrocytic gliosis, phosphorylated, inflammation and reactive microglia as well as synaptic and neuronal victims. The straight combination of AβP into neuronal membranes of memorialized hypothalamic neurons (GT1-7 cells) related with the development of calcium-permeable pores, and also, the elevation of the intracellular calcium concentrations in the GT1-7 cells the distraction of calcium homeostasis by AβP-channels may be the cause of molecular basis of the neurotoxicity of AβP, and the expansion of AD. It is also introduced that the ingredients of membrane lipids can show vital roles in the process of this network development. Our theory may also clarify the appliance of growth of other ‘conformational diseases’, such as type 2 diabetes mellitus or prion disease which part some collective characterize with the AD Enlarged confession of Aβ in those cases resonant the hazard allele. However, the hereditary indication is presently not enough to specify whether βAPP mismetabolism, straight or secondary Aβ neurotoxicity (or its derivatives) are dominant to the AD procedure. The happenings of protein phosphatases strength reduced in the affected neurons in Alzheimer’s disease AD brain, permitting the irregular hyperphosphorylation of tau. Neurofibrillary deterioration can perhaps be subdued by growing the activities of protein phosphatases in the brain of patients with Alzheimer’s disease.


Cadmium is associated with hyperactivity and learning disability, most likely due to a cadmium-induced zinc deficiency. Inhibition of acetylcholine release may also result in hyperkinetic behavior.

Cerebral Hemorrhage

Weakness and hardening of cerebral arteries, due to cadmium toxicity, results in an increased tendency for cerebral hemorrhage


High levels of cadmium are considered to be an important causative factor in hypertension. Cadmium, by impairing kidney function and causing hardening of the arteries, can result in high blood pressure.

Population-based study

Aims of investigations

What is the concentration of cadmium in the blood of normal aging and AD? And to find if there any relation between the concentration of cadmium in blood and cognitive functions.

Blood sampling from subjects

The subjects were from a population-based study, which has been reported in detail elsewhere (Fratigilation et al., 1991, 1992). The project was based on all inhabitants who born 1912 and before and living in areas of Stockholm called kungsholmen in October 1987. There were 2368 individuals 1800 females and 568 males. The whole population was assessed with the Mini-Mental State Examination. Ten ml blood was collected from 29 subjects (21 females and 8 males). The sample collectors were non-smokers. Before collection of blood, the skin of the patient was cleaned with the help of mediswab. Which containing iso-propanol venojet VT 100-H with green stoppers. The tubes turned 10-15 times for mixing. Then 1 ml was transferred to an acid washed tubes with Pasteur pipette and frozen at -20 oC and stored at -80 oC .after 1 week. (Basun et al. , 1994).


Smokers had more cadmium concentration in their blood than non-smokers.

Molecular Mechanism of Cadmium-induced Mental Retardation.

Intellectual disability (ID) is a common neurodevelopmental disorder that is characterized by an intelligence-quotient (IQ) of 70 or below. And also a deficiency in at least two behaviors of adaptive functioning especially when diagnosed at 18 years of age(American Psychiatric Association2000). Especially the deficiency of adaptive functioning includes self-care, judgment, communication, reasoning, and memory loss etc.

Approximately 30% more males are diagnosed with an Intellectual disability than females.

Cadmium (Cd), a toxic heavy metal, which released from cigarette smoking, smelting and the refining of metals, and also burning of chemical fuels also others include municipal wastes. Cadmium can be absorbed in both animals and leads to its accumulation. As cadmium has its half life 15-20 years so it accumulated in the human body in major organs such as kidneys, liver, and even brain and leads to their damages, and its accumulation becomes the cause of or leads to carcinogenesis, immunodepression, and neurodegenerative disorders.

Cadmium can accumulate in the brain also clinical data have shown that Cd in the brain contributes to neurological disorders such as learning disabilities, hyperactivity in children, neurobehavioral defects in

attention, psychomotor speed, and also memory in the workers exposed to Cd. Cd is a possible factor which can cause neurodegenerative disorders, e.g,  amyotrophic lateral sclerosis Alzheimer’s disease, and Parkinson’s disease. Calcium is an intracellular signal which is responsible for

controlling many cellular processes which includes cell survival/death, proliferation, and differentiation.

Elevation of the Cytoplasmic Ca+2 level activates the MAPK and m-TOR.

Also, it is observed that cadmium can disturb the intracellular Ca+2 ions concentration and eventually leads to apoptosis in a variety of cells such as hepatic, kidneys, thyroid cancer cells and also in brain cells which eventually becomes the cause of Mental Retardation. The elevation Ca+2 ions level activate the Mitogen-activated protein kinase MAPK cascade, which is involved in cell signaling and also involve in cell apoptosis, C+2 increased level also activate mammalian Target of rapamycin mTOR and also (P13k)-Akt pathway, ( Baoshan et al. 2011). The activation of MAPK and mTOR control cell death and survival depending upon the stimuli. Also, Cd-induced neuronal apoptosis is partially associated with the activation of t signaling pathways involving the c-Jun N-terminal kinase (JNK) and Akt/mTOR, as well as extracellular signal-regulated kinase 1/2 (Erk1/2) in neuronal (PC12 and SH-SY5Y) cells (Chen 2008).

Cd-induced neuronal toxicity is as a result of induction of Reactive Oxygen Species (ROS).

Under pathological conditions, the excessive amounts of ROS induced by Cd can modify lipids, proteins, and DNA, alter their functions, and also activate the related signaling pathways, so the Cd-induced neurotoxicity is due to generation or induction of ROS. Cd can activate the MAPK pathway by the generation of ROS and which activate Erkt1/2 and JNK and leading to apoptosis of neural cells.


The AD is the main leading cause of dementia, affecting more than 26 million people around worldwide. To enter clinical trials in humans Aβ immunotherapy has started from preclinical studies in transgenic mouse models of the AD. Nevertheless, studies of active and passive Aβ immunotherapies are continuing to go forward, with an estimated total enrollment of more than 9,000 patients. According to the results from preclinical and clinical studies, if patients are immunized before disease onset or in the earliest stages of the disorder it is believed that Aβ immunotherapy has strong potential for preventing AD.

Alzheimer’s disease is a progressive neurodegenerative ailment of the mature, categorized by extensive loss vital cholinergic purpose. Also, the only indicative management verified operative, to date is the use of cholinesterase (ChE) inhibitors to enhance living cholinergic action. And the Cholinesterase inhibitors act on the enzymes that hydrolyze acetylcholine (ACh) and following synaptic release. Investigational proof from the use of agents with enriched choosiness for ChE inhibitors such as rivastigmine and BuChE (cymserine, MF-8622), which have a double-inhibitory action on both BuChE and AChE, designate potential relaxing positive points of preventing both BuChE and AChE in Alzheimer’s disease and associated dementias.

Future directions

For the treatment of Alzheimer disease, many potential therapeutic agents are currently under investigation. Enzymes involved in the formation of β-amyloid and Amyloid precursor protein are thought to contribute to genetic forms of Alzheimer disease; so, interventions to reduce amyloid plaque burden by altering the amyloid metabolism are now being evaluated. To promote clearance of β-amyloid from the central nervous system Immunotherapy is being assessed. Other treatments include resveratrol, (a compound present in the skin of red grapes), which have beneficial effects on aging in mice, and, an N-methyl-D-aspartate receptor antagonist that may also weakly inhibit the acetylcholinesterase, and which may improve cognitive performance and is currently in the trial phase. Agents targeted against tau are also other possible options. Also due to high prevalence, of the fragile X syndrome most therapeutic studies have focused on it. Recently, it was discovered minimally affected individuals with an unmethylated full mutation still produce the FMR1 proteins. So it was concluded that the silencing of the FMR1 gene is caused by the methylation. Due to the extreme genetic heterogeneity, the development of rational therapies for mental retardation disorders is more difficult than for any other type of disorder. Perhaps to develop therapy a more realistic approach would be to increase our insights that, in how mutations in these mental retardation genes lead to disease. Common pathways might be involved in more than a single disorder. Therefore, increasing our vision of the molecular causes of the mental retardation might lead to realistic therapies for mental retardation diseases in the future.


Cadmium a heavy toxic metal which released from different human activities such as smelting and refining of metals and other main source is food, it can be introduced into human body either by direct Cd contaminated environment e.g in workers or by food. As it has a large half life so leading to its accumulation in the different major organs and leads to their damage. Also can accumulate in the brain and lead to apoptosis of neurons, by activating the MAPK and m-TOR pathways. Cd can activate MAPK and m-TOR by disturbing the intercellular Ca+2 ions level in the cytoplasm and activated MAPK can, in turn, activate the JNK pathway, and leads to neurons cells apoptosis. Also, Cd-induced neuronal toxicity is due to oxidative stress by the induction of ROS by Cd. Consequently, Cd-elevated [Ca2+] ions induce ROS and also activates MAPK and mTOR pathways which lead to neuronal cell death.

05 Aug 2018


A random specimen of stool (at least 4 ml or 4 cm³) is collected in a clean, dry, container with a tightly fitting lid (a tin box, plastic box, glass jar, or waxed cardboard box) and transported immediately to the laboratory (this is because trophozoites of Entameba histolytica rapidly degenerate and alter in morphology). About 20-40 grams of formed stool or 5-6 tablespoons of watery stool should be collected. Stool should not be contaminated with urine, water, soil, or menstrual blood. Urine and water destroy trophozoites; the soil will introduce extraneous organisms and also hinder proper examination. Parasites are best detected in warm, freshly passed stools and therefore stools should be examined as early as possible after receipt in the laboratory (preferably within 1 hour of collection). If a delay in the examination is anticipated, the sample may be refrigerated. A fixative containing 10% formalin (for the preservation of eggs, larvae, and cysts) or polyvinyl alcohol (for the preservation of trophozoites and cysts, and for permanent staining) may be used if the specimen is to be transported to a distant laboratory.

Table 1181.1 Differences between amebic and bacillary dysentery
Parameter Amebic dysentery Bacillary dysentery
1. Cause Entamoeba histolytica Shigella (most common)
2. Onset Gradual Acute
3. Fever/vomiting Not significant Significant
4. Appearance of fecal sample Unformed with blood and mucus Unformed with blood, mucus, and pus
5. Microscopic examination of stool    
    • Red cells Clumps Discrete
    • Pus cells Nil or few Numerous
    Macrophages Not seen Many, some with ingested red cells
    • Charcot-Leyden crystals May be present Not seen
    • Trophozoites of E. histolytica Present Not seen
    • Bacteria Many, motile Few, nonmotile
6. Antigen test for E. histolytica Positive Negative
7. Stool culture Negative Positive for Shigella
Table showing the differences between amebic and bacillary dysentery


Entamoeba histolytica

E. histolytica is worldwide in distribution and endemic in tropical and subtropical countries. It is transmitted by the fecal-oral route (ingestion of food or water contaminated by cysts of E. histolytica).

Infection by E. histolytica may be asymptomatic or may cause amebic dysentery or amebic liver abscess. Amebic trophozoites invade the large intestinal mucosa, multiply in the submucosa, spread laterally and produce flask-shaped ulcers. Symptoms include low-grade fever, diarrhea with blood and mucus, weight loss, and cramping abdominal pain. The cecum, ascending colon, and rectosigmoid are commonly affected. Excessive granulation tissue may form in the intestine at the site of lesion (ameboma) to produce constriction, which may be mistaken clinically for a neoplasm.

In some cases, amebae penetrate the portal vessels and are transported to the liver where they form the liver abscess. Amebic abscesses can also form in lungs or brain.

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Life cycle of E. histolytica

Infection is acquired by ingestion of food or water contaminated with infective (quadrinucleate) cysts of E. histolytica. Dissolution of cyst wall in the small intestine occurs with formation of trophozoites. Actively motile trophozoites invade large intestinal mucosa, lodge in the submucosa, multiply, and cause disease (colitis).

Extraintestinal spread to the liver and other sites can occur.

Under unfavorable conditions, encystation of trophozoites leads to the formation of cysts in the intestinal lumen. Cysts are discharged in feces and can survive in moist environmental conditions for weeks to months and propagate the life cycle by the further fecal-oral spread.

Laboratory Diagnosis

1. Identification of trophozoites and cysts on stool examination:

Demonstration of trophozoites of E. histolytica in fecal specimens is required for the diagnosis of amebic dysentery. For diagnosis, at least three fresh stool samples should be examined to increase sensitivity. Trophozoites vary from 15 to 40 μ in diameter. In saline wet mounts, trophozoites show motility in one direction via pseudopodia, which form rapidly. Cytoplasm shows outer transparent ectoplasm and inner finely granular endoplasm. The diagnostic feature of E. histolytica trophozoites is the presence of ingested red cells. The nucleus is visible in the iodine preparation (Figure 1181.1). Fine granules of peripheral nuclear chromatin are evenly distributed along the nuclear membrane. Karyosome is small and centrally placed (Motility is lost in iodine mount).

Figure 1181.1  Uninucleate cyst (left) of E. histolytica and Trophozoite (right). Nuclear chromatin is finely beaded and evenly coats regular nuclear membrane. Karyosome is central. Chromatoid body is long with rounded ends
Figure 1181.1 Uninucleate cyst (left) of E. histolytica and Trophozoite (right). Nuclear chromatin is finely beaded and evenly coats regular nuclear membrane. Karyosome is central. Chromatoid body is long with rounded ends

Cysts of E. histolytica are spherical and measure 10-15 μ in diameter. Nuclei are 1, 2, 3, or 4 and are similar in morphology to trophozoite nucleus (mature cyst contains 4 nuclei). The nuclear membrane is regular and thin with finely granular peripheral chromatin. Karyosome is small and central. Immature cysts may show chromatoid bodies (aggregates of ribosomes) that are oblong structures with rounded ends, and glycogen clumps (Figure 1181.2).

Figure 1181.2 Uninucleate binucleate trinucleate and quadrinucleate cysts of Entamoeba histolytica
Figure 1181.2 Uninucleate, binucleate, trinucleate, and quadrinucleate cysts of Entamoeba histolytica

Entameba dispar is a morphologically identical organism; however, it is non-pathogenic. If red blood cells are identified within trophozoites, then the species is E. histolytica. However, there is no morphologic feature to distinguish between the cysts of these two organisms. Therefore, if only cysts are identified on stool examination, they are reported as “Cysts of E. histolytica/dispar”. Asymptomatic infections with E. histolytica reported in the past are now known to be due to E. dispar. Monoclonal antibodies can distinguish between these two organisms.

Entamoeba histolytica can be definitively identified in saline wet mount if it shows definite directional motility and contains ingested red cells.

It is also necessary to distinguish E. histolytica from other non-pathogenic amebae found in stools like Entamoeba coli, Entamoeba hartmanii, Endolimax nana, and Iodameba butschlii.

Wet mount examination of stool has low sensitivity (25-60%) and also false-positivity due to E. dispar. For identification of trophozoites, stool smears can be prepared and stained with trichrome stain (Figure 1181.3).

Figure 1181.3 Trophozoite of Entamoeba histolytica showing ingested red cells Trichrome stain
Figure 1181.3 Trophozoite of Entamoeba histolytica showing ingested red cells (Trichrome stain)

2. Other findings on stool examination:

Plenty of red cells and very few white cells are helpful in differentiating amebic from bacillary dysentery. Charcot-Leyden crystals may be seen. Differences between amebic and bacillary dysentery are listed in Table 1181.1.

3. Detection of the antigen of E. histolytica in stools:

Direct detection of antigen-specific to E. histolytica is possible by commercially available tests based on enzyme immunoassay. These tests are specific and sensitive (90%) and can differentiate E. histolytica from E. dispar. These tests are indicated if direct stool examination is negative for organisms and intestinal amebiasis is suspected clinically.

4. Detection of DNA specific to E. histolytica:

It is possible by polymerase chain reaction-based assays.

5. Serologic tests:

Serologic tests, which detect antibodies to E. histolytica, are performed to support the diagnosis of invasive amebiasis (i.e. colitis, liver abscess, or ameboma) when organisms cannot be demonstrated on stool examination. Various tests are available like latex agglutination test, indirect hemagglutination test, enzyme immunoassay, and counterimmunoelectrophoresis. Enzyme immunoassay is the method of choice since it is most sensitive and specific. Serologic tests, however, remain positive for many years after infection and thus cannot distinguish between recent and past infections.

6. Endoscopic biopsy of ulcer in the intestine:

This can demonstrate trophozoites of E. histolytica in 50% of cases. Staining with periodic acid Schiff stain facilitates identification of parasites.

Giardia intestinalis (lamblia)

G. intestinalis (lamblia), a pathogenic intestinal protozoan, has a worldwide distribution. It is transmitted by the fecal-oral route and is usually water-borne. Giardia is resistant to chlorine levels in tap water and is commonly found in cold mountain streams. Giardiasis frequently occurs in persons who spend time camping outdoors or in woods and is also called as “Backpacker’s diarrhea” or “beaver fever”. It can cause asymptomatic infection, mild diarrhea, or a severe disease with diarrhea, malabsorption, weight loss and steatorrhea.

Life cycle of Giardia intestinalis (lamblia)

There are two stages in the life cycle, cyst, and trophozoite. After ingestion of cysts, excystation occurs due to the action of gastric acid, and trophozoites are released which migrate to the duodenum and proximal jejunum where they attach to the mucosa and replicate.

Laboratory Diagnosis

1. Demonstration of trophozoites or cysts:

G. lamblia trophozoites are found in fresh liquid stools, particularly in flakes of mucus. They often occur in clusters. Cysts are more likely to be found in formed or loose stools.

Duodenal aspirates may be obtained if repeated fecal examinations are negative for G. lamblia and there is a strong clinical suspicion of giardiasis. However, the test is invasive and is usually not necessary for diagnosis.

Trophozoites of G. lamblia are pear-shaped, 12-15 μ in diameter, have 4 pairs of flagella, 2 large and oval nuclei, 2 axonemes (axial filaments of flagella), and 1 or 2 curved median bodies. Motility is likened to that of “falling leaf”.

Cysts of G. lamblia are 8-12 μ in diameter, oval, and contain 4 nuclei, axonemes, median bodies, and remains of flagella (Figure 1181.4).

Figure 1181.4 Cyst and trophozoite of Giardia lamblia
Figure 1181.4 Cyst and trophozoite of Giardia lamblia

2. Detection of the antigen of G. lamblia in stool sample:

The antigen of G. lamblia can be demonstrated by enzyme immunoassay technique with high sensitivity (90-99%) and specificity (95-100%). This test can be used as the initial test for diagnosis of giardiasis; however, stool examination is still important for detection of other concomitant parasite infections.

3. Direct fluorescent antibody assay:

This test is available commercially in a kit form and is highly sensitive and specific. Cysts are labeled with immunofluorescent antibodies and are detected under the fluorescence microscope.


Isospora belli, Cryptosporidium parvum, and Cyclospora cayetanensis are human intestinal coccidia. They have a worldwide distribution. Transmission is by the fecal-oral route (ingestion of infective oocysts). These protozoan organisms cause self-limited, mild diarrheal illness; however, in immunocompromised patients (such as patients with acquired immunodeficiency syndrome) they can induce severe and protracted diarrhea, which may sometimes be life-threatening.

Life cycle of Coccidia

Ingestion of infective oocysts by humans leads to infection. The release of sporozoites from oocysts occurs which infect intestinal epithelial cells. Sporozoites multiply within epithelial cells with formation of merozoites (asexual reproduction by fission or schizogony), which infect other epithelial cells. Some merozoites develop into male and female gametes. Fertilization of male and female gametes produces a zygote.

Oocyst is formed by encystation around the conjugating gametes. Sporozoites form within oocysts by sexual reproduction or sporogony. Oocysts are excreted in feces and contaminate food or water.

Laboratory Diagnosis

1. Examination of stools for the demonstration of oocysts of I. belli, C. parvum, or C. cayetanensis:

Isospora belli: Oocysts of I. belli can usually be found in direct wet mounts of feces (unstained). Formalin-ether concentration technique may sometimes be necessary. Oocysts of I. belli are oval and about 32 × 16 μ in size. Immature oocysts contain a granular zygote. Mature oocysts contain two sporocysts, each with four sporozoites. With modified Ziehl-Neelsen stain (on a fecal smear prepared from the sediment after formalin-ether concentration), oocysts stain uniform red-pink. Under ultraviolet light, oocysts show autofluorescence.

Cryptosporidium parvum: Oocysts of C. parvum are difficult to demonstrate in direct fecal wet mounts. They are demonstrated either by modified Ziehl-Neelsen staining of concentrated fecal smear or by immunofluorescence technique. They are 4-6 μ in size, round to oval, and stain pink-red.

Cyclospora cayetanensis: In direct wet mounts of feces, oocysts measure 8-10 μ in diameter, and contain a cluster of refractile globules (morula-like appearance). With modified Ziehl-Neelsen stain, they appear similar to C. parvum but are larger. Under ultraviolet light (365 nm), oocysts show intense blue autofluorescence.

2. Detection of antigen in stool samples:

Enzyme immunoassay for detection of specific antigen of C. parvum is available. It is more sensitive and specific than Ziehl-Neelsen staining.

3. Direct fluorescent antibody assay:

This assay is available for Cryptosporidium parvum and is highly sensitive and specific. Oocysts of Cryptosporidium labeled with fluorescent antibody are readily detected under the fluorescence microscope.


Microsporidia are obligate intracellular protozoa, which cause opportunistic infection in immunocompromised patients leading to persistent diarrhea and weight loss. Common species causing infection in humans are Enterocytozoon bieneusi, Encephalitozoon intestinalis, and Encephalitozoon hellem.

Transmission of infection is by ingestion of spores. The organisms develop and multiply in intestinal cells and form infective spores; rupture of host cells releases spores some of which infect newer cells while others are excreted in feces.

Some microsporidia can cause keratoconjunctivitis, hepatitis, peritonitis, respiratory infection, and kidney disease. Microsporidia cannot be demonstrated on wet mounts because of their very small size.

Laboratory Diagnosis

1. Modified trichrome stain of stool sample:

Spores are very small (1-5 μ), stain red, and may show a transverse band.

2. Small intestinal biopsy for the demonstration of spores within intestinal cells.


Ascaris lumbricoides (Roundworm)

This is the most common helminthic infection in humans. Children are more commonly affected than adults. Mode of transmission is the fecal-oral route (ingestion of infective eggs). Adult worms live in the small intestine (duodenum and jejunum) of the host. Eggs are laid by adult female worms (about 200,000 per day), which are excreted in feces. Eggs can remain viable in the soil for many years. Contamination can occur when untreated human feces are used as a fertilizer or by soiling of hands of playing children. Adult worms can live in the intestine for 1-2 years.

Life cycle of Ascaris lumbricoides (Roundworm)

Infection is acquired by ingestion of infective eggs via contaminated food or hands. Eggs hatch to release larvae in the intestine. Larvae penetrate the mucosa and enter the bloodstream. Larvae circulate, reach lungs and penetrate alveolar walls to enter the respiratory tree.

Larvae migrate up the trachea to the epiglottis from where they are swallowed. Maturation of larvae to adult worms occurs in the small intestine. Female worms lay down eggs, which are excreted in feces. Eggs become embryonated (infective) in 4-6 weeks in a favorable environment.

Clinical Features

  • Asymptomatic if the infection is light.
  • Loeffler’s syndrome: Migration of larvae through the lungs can induce a cough, wheezing, eosinophilia, and bilateral, irregular pulmonary densities.
  • Local effects: These include abdominal pain, diarrhea, intestinal obstruction due to a large mass of worms, and intestinal perforation. Sometimes worms can invade pancreatic duct or common bile duct and cause obstruction; this can lead to pancreatitis or obstructive jaundice respectively. From the bile duct, adult worms can reach the liver and cause an abscess. Adult worms can migrate to the appendix to cause appendicitis.
  • Malabsorption

Laboratory Diagnosis

1. Demonstration of eggs of A. lumbricoides:

Diagnosis of A. lumbricoides infection is made by demonstration of eggs on stool examination. Eggs can be demonstrated in the direct wet mount of feces in moderate to heavy infections. The recommended procedure is formol-ethyl acetate sedimentation technique for the concentration of eggs. In feces, four types of eggs are found: fertilized (double-shelled or decorticated) and unfertilized (double-shelled or decorticated).

Fertilized eggs: These are oval, yellow-brown, and about 70 μ × 50 μ in size. They have outer and inner shells. The outer shell is uneven, brown (due to staining by bile), and rough (mamillated), while the inner shell is thick, smooth, and colorless. The egg contains a single central granular mass (fertilized ovum).

Unfertilized eggs: Single female worms discharge these eggs. They are slightly larger and more elongated than the fertilized eggs (90 μ in length). The outer shell is dark brown and more irregular, while the inner shell is thinner. This egg is filled with a mass of large refractile granules (Figure 1181.5).

Decorticated eggs do not have the outer uneven shell and resemble the hookworm eggs.

Figure 1181.5 Unfertilized and fertilized eggs of Ascaris lumbricoides
Figure 1181.5 Unfertilized and fertilized eggs of Ascaris lumbricoides

2. Identification of adult worms:

Occasionally adult worms are passed spontaneously in the feces and brought to the laboratory for identification. Adult Ascaris worms are cylindrical or round, pinkish, and measure about 15 cm (male) or 30 cm (female) in length. Diameter is about 0.5 cm and the tail is curved (male) or straight (female). There are three lips at the anterior end (mouth).


The hookworms are Ancylostoma duodenale (old world hookworm) and Necator americanus (new world hookworm).

Life cycle of hookworms

Infection occurs when there is penetration of the skin of foot by filariform larvae present in the soil. Larvae enter the circulation, and through veins are carried to the heart and then reach lungs, migrate up the respiratory tree and are swallowed. Maturation of larvae to the adult worms occurs in the small intestine. Adult worms attach to the mucosa and suck blood. Adult female worms produce eggs, which are excreted in feces. Rhabditiform larvae are released from eggs into the soil and mature into infective filariform larvae. Both A. duodenale and N. americanus infection are acquired when infective filariform larvae penetrate the skin. A. duodenale infection is also acquired by ingestion of infective larvae.

Clinical Features

Hookworm infection can cause:

  • “Ground itch”: This is inflammation and marked itching on the skin at the site of larval penetration.
  • Loeffler’s syndrome: This is due to migration of larvae through the lungs.
  • Iron deficiency anemia due to chronic blood loss: This is a well-known and most common complication of hookworm infection. Adult worms attach themselves to the small intestinal mucosa by teeth-like structures or cutting plates, and suck blood. They then change their sites of attachment (every 4-8 hours) while blood continues to ooze from the previous site. One adult A. duodenale causes loss of 0.15 ml of blood while one N. americanus causes loss of 0.03 ml per day.
  • Abdominal pain and diarrhea if worm load is high.

Laboratory Diagnosis

1. Demonstration of hookworm eggs:

Diagnosis is based on the identification of hookworm eggs on stool examination. The technique of formol-ethyl acetate sedimentation is preferred; if not available, a direct wet mount of a fecal sample can demonstrate eggs in moderate to heavy infections. Eggs of A. duodenale and N. americanus are morphologically similar. They are 50-75 μ in length and 40 μ in width, oval, colorless, and have a thin shell. In fresh stools, eggs show 4-8 gray, granular cells (Figure 1181.6). If the stool is more than 12 hours old, eggs will show a rhabditiform larva folded upon itself. Such an egg is called as embryonated. If feces are more than 24 hours old, then free rhabditiform larvae will be seen. This should be differentiated from larvae of Strongyloides stercoralis (buccal cavity of hookworm larva is longer).

Figure 1181.6 Hookworm egg in fresh stools. Egg in oval shape with a thin shell, has a clear space between wall and developing cleavage, and contains granular cells
Figure 1181.6 Hookworm egg in fresh stools. Egg in an oval shape with a thin shell, has a clear space between the wall and developing cleavage, and contains granular cells

2. Other laboratory features:

Blood examination often shows eosinophilia. Microcytic hypochromic anemia develops due to chronic blood loss. Test for occult blood in stools is positive.

Trichuris trichiura

Infection is acquired by ingestion of infective eggs. Larvae, which are released, develop into adult worms and attach to the mucosa. Released eggs are excreted in feces, and mature in the soil to the infective stage under suitable conditions. Heavy infection can cause diarrhea with blood and mucus in stools, iron deficiency anemia, or rectal prolapse.

Diagnosis depends on identification of typical eggs on stool examination. Eggs measure 50 × 25 μ in size, are yellow-brown and barrel-shaped. A rounded, transparent plug is present at both poles (Figure 1181.7). Eggs contain central, uniformly granular mass. Eggs are often quantitated to assess the severity of an infection.

Figure 1181.7 Egg of Trichuris trichiura in iodine wet mount
Figure 1181.7 Egg of Trichuris trichiura in iodine wet mount

Strongyloides stercoralis

Life cycle of Strongyloides stercoralis

The life cycle is more complex than that of other nematodes. Penetration of skin by infective filariform larvae in the soil causes infection. Larvae enter the circulation and migrate to the lungs, penetrate the alveolar spaces, move up the trachea, and are swallowed. Maturation to adult worms occurs in the small intestine. Female worms lay down eggs (parthenogenesis). Eggs hatch to release rhabditiform larvae in the small intestine, which are excreted along with feces (Sometimes, rhabditiform larvae can mature into filariform larvae, which penetrate mucosa, or perianal skin and enter the circulation; this is called as autoinfection). Maturation of rhabditiform larvae to infective filariform larvae occurs in soil, which can penetrate the skin and cause infection. If this does not happen, larvae develop into adult male and female worms which mate and lay down eggs, from which rhabditiform larvae are released which further mature into infective filariform larvae.

Clinical Features

  • Redness and itching at the site of penetration of filariform larva.
  • Loeffler’s syndrome due to the migration of the larva through the lungs.
  • Heavy infection can cause abdominal pain, diarrhea, and malabsorption.
  • Chronic infection causes abdominal pain, diarrhea, and urticaria.
  • In immunocompromised persons, potentially fatal hyper-infection (secondary to auto-infection) can occur causing severe pneumonia, neurologic complications, abdominal pain, shock, and septicemia.

Laboratory Diagnosis

Identification of larvae of S. stercoralis:

Diagnosis of S. stercoralis infection depends on the demonstration of rhabditiform larvae in fresh stool specimens. Eggs of S. stercoralis are rarely seen in stool samples because they hatch and release rhabditiform larvae in the intestine. Rhabditiform larvae are 200-300 μ in length and 15 μ in width and are actively motile. They have two esophageal swellings, a prominent genital primordium, and a short buccal cavity. Sometimes, in old fecal samples, rhabditiform larvae of hookworms are seen which resemble those of S. stercoralis; the differentiating feature is the longer buccal cavity of the former.

Excretion of larvae is often irregular and their number may be few. Therefore, a fecal examination may yield the negative result. In suspected cases, concentration technique (formol-ethyl acetate) is helpful.

Duodenal fluid can be aspirated for detection of larvae or Entero-test (String test) can be performed. (Entero-test: A commercially available gelatin capsule consists of a textured string. One end of the string is attached or taped to the cheek and the capsule is then swallowed. The end of the string reaches and is exposed in the duodenum after several hours. After removal, the terminal part of the string should be bile-stained. The mucus from the end of the string is wiped onto a glass slide and examined for larvae). In disseminated infection, larvae may be detected in sputum.

Enzyme immunoassay test that detects IgG antibodies to S. stercoralis is available and is indicated if the organism is not detected in feces, duodenal aspirate, or string test and clinical suspicion is strong. It cannot differentiate between recent and past infection.

Enterobius vermicularis

E. vermicularis is also called as pinworm, seatworm, or oxyurids. It is distributed worldwide. Infection is common in children. Mode of transmission is ingestion of food or water contaminated with infective eggs through fingers.

Life cycle of E. vermicularis

After ingestion, eggs hatch to release larvae in the intestine. Larvae mature to the adult worms in the cecum or appendix. Female worms migrate at night to the perianal skin to deposit up to 15,000 eggs. Marked irritation at the site leads to contamination of fingers through scratching which causes self-infection by transferring eggs to the mouth. Enterobiasis can also be acquired by handling contaminated clothes, linen, etc.

Clinical Features

Intense nocturnal perineal or perianal itching is usual. Acute appendicitis can occur due to the presence of the worm in the appendix. Sometimes, the worm can invade female genital tract leading to vulvovaginitis, and formation of pelvic and peritoneal granulomas.

Special technique for collection and demonstration of pinworm eggs: Adult female pinworm migrates at night from the intestine (cecum) to the perianal skin and deposits eggs. Pinworm eggs are, therefore, detected in perianal skin folds and are often not found on routine stool examination. Pinworm eggs can be collected either by a transparent adhesive tape (“cellophane tape test”) or by anal swab. Specimen should preferably be collected late into the night or early morning before patient passes urine, feces, or takes a bath.

A transparent adhesive tape is folded over the end of a glass slide, spoon handle or a wooden tongue depressor (sticky surface outwards). Patient’s buttocks are separated and the slide or spoon handle covered with tape is pressed over the perianal skin at many sites. The tape is then spread over a glass slide with adhesive side down and pressed flat onto the slide surface. Slide covered with tape is then examined under the microscope.

In another method, a cotton swab is rubbed around the anus and then rinsed in a test tube containing 0.5 ml saline. The fluid is drawn in a pipette; a drop is placed on a glass slide and observed under the microscope with reduced illumination.

Laboratory Diagnosis

Diagnosis depends on the demonstration of eggs in samples collected from perianal skin (transparent adhesive tape method) or demonstration of adult worms. Eggs of E. vermicularis measure 60 μ × 30 μ in size, are oval and flattened on one side. They are colorless, transparent with a double-lined smooth shell, and contain a small granular mass (Figure 1181.8) or a larva. Adult pinworms may be recovered from perianal skin folds (by adhesive tape) or may be found in children’s feces. They are white, motile, and small in size (male: 0.5 cm; female: 1 cm).

Figure 1181.8 (A) Enterobius eggs (B) Enterobius eggs collected by transparent tape method
Figure 1181.8 (A) Enterobius eggs, (B) Enterobius eggs collected by transparent tape method

Taenia solium

T. solium occurs mainly in India, Pakistan, China, S. Africa, and Latin America. It is transmitted by ingestion of raw or undercooked pork containing infective cysticercus larvae (cysticercus cellulose).

Life cycle of T. solium

Infection is acquired by ingestion of raw or undercooked pork containing infective encysted cysticercus larva by a man who is a definitive host. Scolex of cysticercus is freed and attaches to the wall of the intestine by its suckers and hooks. Development of cysticercus into an adult tapeworm occurs by addition of multiple segments or proglottids to the scolex. Length of the adult tapeworm is about 2-7 meters. Each proglottid is a functional hermaphroditic reproductive unit, which produces numerous eggs. The egg-filled segment at the end of the worm detaches itself from the worm and releases eggs in feces; segment is also excreted. Eggs contaminate the soil and are ingested by the pigs (intermediate hosts) while feeding. Embryo (released from the egg) penetrates the intestinal wall of the pig and is carried through the bloodstream to the muscles where it develops into infective cysticercus larvae.

Man can become an intermediate host if he eats food contaminated with eggs or if there is self-contamination (through contaminated fingers). In such an event, embryo enters the bloodstream and cysticercus develops at any body site.

Clinical Features

  • Intestinal infection: Clinical features are usually insignificant. The patient may notice the passage of a flat segment of the worm in feces.
  • Cysticercosis: This occurs if the man accidentally ingests food contaminated with T. solium eggs (or if there is autoinfection). Nodules containing cysticercus develop in skeletal muscle, subcutaneous tissue, heart, liver, brain, etc. Cysticercus (or bladder worm) is a small cyst (< 1.5 cm) containing clear fluid and inverted scolex.
  • Involvement of brain (neurocysticercosis) can cause seizures (neurocysticercosis is a common cause of epilepsy in endemic areas in children), raised intracranial tension (due to obstruction to cerebrospinal fluid flow by intraventricular cysts), psychiatric disturbances, and localizing signs; sometimes sudden death can occur.

Laboratory Diagnosis

1. Examination of feces:

  1. Identification of eggs: Morphologically, eggs of T. solium and T. saginata are identical. The distinction between the two species requires examination of proglottids or scolices. Egg measures 30-40 μ in diameter, is round to oval and has a thick, brown wall with transverse lines. The egg contains an embryo, which is a round granular mass containing 3 pairs of hooklets and surrounded by a fine membrane (Figure 1181.9). Occasionally, the egg is enclosed in a clear sac. Eggs are discharged intermittently by the tapeworm and therefore may not be detected easily. Repeated stool examinations and formol-ether concentration technique are often required for their demonstration.
  2. Identification of gravid segments or proglottids: This allows identification of species. The segment is flattened between two glass slides and examined under a magnifying glass. Gravid segment is 13 mm × 8 mm in size, translucent, and pale blue. It has a central uterine stem with 8-13 lateral branches. (Uterine branches are >13 in T. saginata).
  3. Identification of scolex (head): Scolex of a tapeworm is very small (pinhead size) and is rarely seen. When examined with a magnifying glass, scolex of T. solium shows 4 suckers and a crown of hooklets.
Figure 1181.9 Egg of Taenia solium or saginata
Figure 1181.9 Egg of Taenia solium/saginata

2. Diagnosis of cysticercosis:

Cysticercosis can be diagnosed by serologic tests, radiologic studies, and biopsy of the lesion.

Indirect hemagglutination assay has the sensitivity of about 80%. A titer of ≥ 1:64 indicates cysticercosis. Newer glycoprotein immunoblot assay is more sensitive and specific for the diagnosis of neurocysticercosis. X-ray is helpful in detecting calcified cysts. Computed tomography scans are helpful in diagnosing neurocysticercosis.

Taenia saginata

T. saginata (beef tapeworm) has the worldwide distribution with particularly high prevalence in the Middle East, Africa, Asia, and Latin America. Mode of transmission is eating raw or undercooked beef (containing infective cysticercus bovis larvae).

Life cycle is similar to that of T. solium except (i) animal host is cattle, (ii) eggs are not infectious to humans and therefore human cysticercosis does not occur after ingestion of eggs, and (iii) segments of T. saginata also migrate to the perianal skin and deposit eggs.

Clinical Features

These are usually insignificant. Sometimes abdominal pain and diarrhea can occur.

Laboratory Diagnosis

  1. Identification of eggs: Eggs of T. saginata can be identified in feces and perianal skin. They are morphologically similar to those of T. solium.
  2. Identification of gravid segments: Segments measure 20 mm × 6 mm in size, and are ivory white. They contain a central uterine stem with more than 13 side branches (i.e. 15-20 branches).
  3. Identification of head or scolex: Scolex of T. saginata has 4 suckers but no hooklets. It measures 2 mm in width. Various laboratory tests for diagnosis of parasitic infection of intestine are summarized in Table 1181.2.
Table 1181.2 Summary of laboratory tests for diagnosis of intestinal parasites
Test Use
1. Direct saline mount Trophozoites, cysts, ova, and larvae
2. Direct iodine mount Protozoal cysts
3. Faecal concentration Recovery of protozoal cysts, helminth ova and larvae
4. Cellophane tape technique Ova of Enterobius vermicularis
5. Trichrome stain of fecal smear Protozoal cysts and trophozoites
6. AFB stain of fecal smear Oocysts of Cryptosporidium, Cyclospora, and Isospora
7. Detection of antigen in random stool sample E. histolytica, G. lamblia, Cryptosporidium
8. Molecular methods based on polymerase chain reaction on stool sample E. histolytica, G. lamblia, Cryptosporidium, Microsporidia, Cyclospora
9. Serologic methods E. histolytica, S. stercoralis, Cysticercus
Table showing the summary of laboratory tests for diagnosis of intestinal parasites
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