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Urinary Tract Infection

Urinary tract infection

Classification and external resources

Multiple white cells seen in the urine of a person with a urinary tract infection via microscopy










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A urinary tract infection (UTI) is a bacterial infection that affects part of the urinary tract. When it affects the lower urinary tract it is known as a simple cystitis (a bladder infection) and when it affects the upper urinary tract it is known as pyelonephritis (a kidney infection). Symptoms from a lower urinary tract include painful urination and either frequent urination or urge to urinate (or both), while those of pyelonephritis include fever and flank pain in addition to the symptoms of a lower UTI. In the elderly and the very young, symptoms may be vague or non specific. The main causal agent of both types is Escherichia coli, however other bacteria, viruses or fungi may rarely be the cause.

Urinary tract infections occur more commonly in women than men, with half of women having at least one infection at some point in their lives. Recurrences are common. Risk factors include female anatomy, sexual intercourse and family history. Pyelonephritis, if it occurs, usually follows a bladder infection but may also result from a blood borne infection. Diagnosis in young healthy women can be based on symptoms alone. In those with vague symptoms, diagnosis can be difficult because bacteria may be present without there being an infection. In complicated cases or if treatment has failed, a urine culture may be useful. In those with frequent infections, low dose antibiotics may be taken as a preventative measure.

In uncomplicated cases, urinary tract infections are easily treated with a short course of antibiotics, although resistance to many of the antibiotics used to treat this condition is increasing. In complicated cases, longer course or intravenous antibiotics may be needed, and if symptoms have not improved in two or three days, further diagnostic testing is needed. In women, urinary tract infections are the most common form of bacterial infection with 10% developing urinary tract infections yearly.


Signs and symptoms



Urine may contain pus (a condition known as pyuria) as seen from a person with sepsis due to a urinary tract infection.

Lower urinary tract infection is also referred to as a bladder infection. The most common symptoms are burning with urination and having to urinate frequently (or an urge to urinate) in the absence of vaginal discharge and significant pain.[1] These symptoms may vary from mild to severe[2] and in healthy women last an average of six days.[3] Some pain above the pubic bone or in the lower back may be present. People experiencing an upper urinary tract infection, or pyelonephritis, may experience flank pain, fever, or nausea and vomiting in addition to the classic symptoms of a lower urinary tract infection.[2] Rarely the urine may appear bloody[4] or contain visible pyuria (pus in the urine).[5]

In children

In young children, the only symptom of a urinary tract infection (UTI) may be a fever. Because of the lack of more obvious symptoms, when females under the age of two or uncircumcised males less than a year exhibit a fever, a culture of the urine is recommended by many medical associations. Infants may feed poorly, vomit, sleep more, or show signs of jaundice. In older children, new onset urinary incontinence (loss of bladder control) may occur.[6]

In the elderly

Urinary tract symptoms are frequently lacking in the elderly.[7] The presentations may be vague with incontinence, a change in mental status, or fatigue as the only symptoms.[2] While some present to a health care provider with sepsis, an infection of the blood, as the first symptoms.[4] Diagnosis can be complicated by the fact that many elderly people have preexisting incontinence or dementia.[7]


E. coli is the cause of 80–85% of urinary tract infections, with Staphylococcus saprophyticus being the cause in 5–10%.[1] Rarely they may be due to viral or fungal infections.[8] Other bacterial causes include: Klebsiella, Proteus, Pseudomonas, and Enterobacter. These are uncommon and typically related to abnormalities of the urinary system or urinary catheterization.[4] Urinary tract infections due to Staphylococcus aureus typically occurs secondary to blood born infections.[2]


In young sexually active women, sexual activity is the cause of 75–90% of bladder infections, with the risk of infection related to the frequency of sex.[1] The term “honeymoon cystitis” has been applied to this phenomenon of frequent UTIs during early marriage. In post-menopausal women, sexual activity does not affect the risk of developing a UTI. Spermicide use, independent of sexual frequency, increases the risk of UTIs.[1]

Women are more prone to UTIs than men because, in females, the urethra is much shorter and closer to the anus.[9] As a woman’s estrogen levels decrease with menopause, her risk of urinary tract infections increases due to the loss of protective vaginal flora.[9]

Urinary catheters

Urinary catheterization increases the risk for urinary tract infections. The risk of bacteriuria (bacteria in the urine) is between three to six percent per day and prophylactic antibiotics are not effective in decreasing symptomatic infections.[9] The risk of an associated infection can be decreased by catheterizing only when necessary, using aseptic technique for insertion, and maintaining unobstructed closed drainage of the catheter.[10][11][12]


A predisposition for bladder infections may run in families. Other risk factors include diabetes,[1] being uncircumcised, and having a large prostate.[2] Complicating factors are rather vague and include predisposing anatomic, functional, or metabolic abnormalities. A complicated UTI is more difficult to treat and usually requires more aggressive evaluation, treatment and follow-up.[13] In children UTIs are associated with vesicoureteral reflux (an abnormal movement of urine from the bladder into ureters or kidneys) and constipation.[6]

Persons with spinal cord injury are at increased risk for urinary tract infection in part because of chronic use of catheter, and in part because of voiding dysfunction.[14] It is the most common cause of infection in this population, as well as the most common cause of hospitalization.[14] Additionally, use of cranberry juice or cranberry supplement appears to be ineffective in prevention and treatment in this population.[15]


The bacteria that cause urinary tract infections typically enter the bladder via the urethra. However, infection may also occur via the blood or lymph. It is believed that the bacteria are usually transmitted to the urethra from the bowel, with females at greater risk due to their anatomy. After gaining entry to the bladder, E. Coli are able to attach to the bladder wall and form a biofilm that resists the body’s immune response.[4]


A number of measures have not been confirmed to affect UTI frequency including: the use of birth control pills or condoms, urinating immediately after intercourse, the type of underwear used, personal hygiene methods used after urinating or defecating, or whether a person typically bathes or showers.[1] There is similarly a lack of evidence surrounding the effect of holding one’s urine, tampon use, and douching.[9]

In those with frequent urinary tract infections who use spermicide or a diaphragm as a method of contraception, they are advised to use alternative methods.[4] Cranberry (juice or capsules) may decrease the incidence in those with frequent infections,[16][17] but long-term tolerance is an issue[16] with gastrointestinal upset occurring in more than 30%.[18] Twice daily use may be superior to once daily use.[19] As of 2011, intravaginal probiotics require further study to determine if they are beneficial.[4] Condom use without spermicide or use of birth control pills does not increase the risk of uncomplicated urinated tract infection.[20]


For those with recurrent infections, a prolonged course of daily antibiotics is effective.[1] Medications frequently used include nitrofurantoin and trimethoprim/sulfamethoxazole.[4] Methenamine is another agent frequently used for this purpose as in the bladder where the acidity is low it produces formaldehyde to which resistance does not develop.[21] In cases where infections are related to intercourse, taking antibiotics afterwards may be useful.[4] In post-menopausal women, topical vaginal estrogen has been found to reduce recurrence. As opposed to topical creams, the use of vaginal estrogen from pessaries has not been as useful as low dose antibiotics.[22] A number of vaccines are in development as of 2011.[4]

In children

The evidence that preventative antibiotics decrease urinary tract infections in children is poor.[23] However recurrent UTIs are a rare cause of further kidney problems if there are no underlying abnormalities of the kidneys, resulting in less than a third of a percent (0.33%) of chronic kidney disease in adults.[24]




Multiple bacilli (rod-shaped bacteria, here shown as black and bean-shaped) shown between white blood cells in urinary microscopy. These changes are indicative of a urinary tract infection.

In straightforward cases, a diagnosis may be made and treatment given based on symptoms alone without further laboratory confirmation. In complicated or questionable cases, it may be useful to confirm the diagnosis via urinalysis, looking for the presence of urinary nitrites, white blood cells (leukocytes), or leukocyte esterase. Another test, urine microscopy, looks for the presence of red blood cells, white blood cells, or bacteria. Urine culture is deemed positive if it shows a bacterial colony count of greater than or equal to 103 colony-forming units per mL of a typical urinary tract organism. Antibiotic sensitivity can also be tested with these cultures, making them useful in the selection of antibiotic treatment. However, women with negative cultures may still improve with antibiotic treatment.[1] As symptoms can be vague and without reliable tests for urinary tract infections, diagnosis can be difficult in the elderly.[7]


A urinary tract infection may involve only the lower urinary tract, in which case it is known as a bladder infection. Alternatively, it may involve the upper urinary tract, in which case it is known as pyelonephritis. If the urine contains significant bacteria but there are no symptoms, the condition is known as asymptomatic bacteriuria.[2] If a urinary tract infection involves the upper tract, and the person has diabetes mellitus, is pregnant, is male, or immunocompromised, it is considered complicated.[3][4] Otherwise if a woman is healthy and premenopausal it is considered uncomplicated.[3] In children when a urinary tract infection is associated with a fever, it is deemed to be an upper urinary tract infection.[6]

In children

To make the diagnosis of a urinary tract infection in children, a positive urinary culture is required. Contamination poses a frequent challenge depending on the method of collection used, thus a cutoff of 105 CFU/mL is used for a “clean-catch” mid stream sample, 104 CFU/mL is used for catheter-obtained specimens, and 102 CFU/mL is used for suprapubic aspirations (a sample drawn directly from the bladder with a needle). The use of “urine bags” to collect samples is discouraged by the World Health Organization due to the high rate of contamination when cultured, and catheterization is preferred in those not toilet trained. Some, such as the American Academy of Pediatrics recommends renal ultrasound and voiding cystourethrogram (watching a person’s urethra and urinary bladder with real time x-rays while they urinate) in all children less than two year old who have had a urinary tract infection. However, because there is a lack of effective treatment if problems are found, others such as the National Institute for Clinical Excellence only recommends routine imaging in those less than six month old or who have unusual findings.[6]

Differential diagnosis

In women with cervicitis (inflammation of the cervix) or vaginitis (inflammation of the vagina) and in young men with UTI symptoms, a Chlamydia trachomatis or Neisseria gonorrheae infection may be the cause.[2][25] Vaginitis may also be due to a yeast infection.[26] Interstitial cystitis (chronic pain in the bladder) may be considered for people who experience multiple episodes of UTI symptoms but urine cultures remain negative and not improved with antibiotics.[27] Prostatitis (inflammation of the prostate) may also be considered in the differential diagnosis.[28]


The main stay of treatment is antibiotics. Phenazopyridine is occasionally prescribed during the first few days in addition to antibiotics to help with the burning and urgency sometimes felt during a bladder infection.[29] However, it is not routinely recommended due to safety concerns with its use, specifically an elevated risk of methemoglobinemia (higher than normal level of methemoglobin in the blood).[30] Acetaminophen (paracetamol) may be used for fevers.[31]

Women with recurrent simple UTIs may benefit from self-treatment upon occurrence of symptoms with medical follow-up only if the initial treatment fails. A prescription for antibiotics can be delivered to a pharmacist by phone.[1]


Giardia lamblia


Giardia cell, SEM

Scientific classification














G. lamblia

Binomial name

Giardia intestinalis
(Lambl, 1859) Kofoid & Christiansen, 1915


Lamblia intestinalis
Giardia duodenalis

Giardia lamblia (synonymous with Giardia intestinalis, Lamblia intestinalis and Giardia duodenalis) is a flagellated protozoan parasite that colonizes and reproduces in the small intestine, causing giardiasis. The Giardia parasite attaches to the epithelium by a ventral adhesive disc, and reproduces via binary fission.[1] Giardiasis does not spread via the bloodstream, nor does it spread to other parts of the gastro-intestinal tract, but remains confined to the lumen of the small intestine.[2] Giardia trophozoites absorb their nutrients from the lumen of the small intestine, and are anaerobes. If the organism is split and stained, it has a very characteristic pattern that resembles a familiar “smiley face” symbol. Chief pathways of human infection include ingestion of untreated sewage, a phenomenon particularly common in many developing countries;[3] contamination of natural waters also occurs in watersheds where intensive grazing occurs.



Giardia infects humans, but is also one of the most common parasites infecting cats, dogs and birds. Mammalian hosts also include cows, beavers, deer, and sheep.


Giardia infection can occur through ingestion of dormant microbial cysts in contaminated water, food, or by the faecal-oral route (through poor hygiene practices). The cyst can survive for weeks to months in cold water,[4] and therefore can be present in contaminated wells and water systems, especially stagnant water sources such as naturally occurring ponds, storm water storage systems, and even clean-looking mountain streams. They may also occur in city reservoirs and persist after water treatment, as the cysts are resistant to conventional water treatment methods such as chlorination and ozonolysis.[4] Zoonotic transmission is also possible, and therefore Giardia infection is a concern for people camping in the wilderness or swimming in contaminated streams or lakes, especially the artificial lakes formed by beaver dams (hence the popular name for giardiasis, “Beaver Fever”).

In addition to waterborne sources, fecal-oral transmission can also occur, for example in day care centers, where children may have poor hygiene practices. Those who work with children are also at risk of being infected, as are family members of infected individuals. Not all Giardia infections are symptomatic, and many people can unknowingly serve as carriers of the parasite.

Life cycle



Parasite life cycle.

The life cycle begins with a non infective cyst being excreted with the feces of an infected individual. The cyst is hardy, providing protection from various degrees of heat and cold, desiccation, and infection from other organisms. A distinguishing characteristic of the cyst is four nuclei and a retracted cytoplasm. Once ingested by a host, the trophozoite emerges to an active state of feeding and motility. After the feeding stage, the trophozoite undergoes asexual replication through longitudinal binary fission. The resulting trophozoites and cysts then pass through the digestive system in the faeces. While the trophozoites may be found in the faeces, only the cysts are capable of surviving outside of the host.

Distinguishing features of the trophozoites are large karyosomes and lack of peripheral chromatin, giving the two nuclei a halo appearance. Cysts are distinguished by a retracted cytoplasm. This protozoan lacks mitochondria, although the discovery of the presence of mitochondrial remnants organelles in one recent study “indicate that Giardia is not primitively amitochondrial and that it has retained a functional organelle derived from the original mitochondrial endosymbiont”[5] This organelle is now termed a mitosome.

Intracellular metabolism and biochemistry

Giardia relies on glucose as its major energy source and breaks glucose down into ethanol, acetate and carbon dioxide.[6] However, it can also use arginine as an energy source.[7] Giardia possesses unique biochemical pathways that suggest that it diverged from other eukaryotes at an early stage in evolution.[7]

B vitamins and bile salts, as well as glucose, are necessary for Giardia to survive, and a low-carbohydrate diet was shown in mice to reduce the number of Giardia organisms present.[8]

Manifestation of infection



Fig.Giardia lamblia seen in a cytologic preparation (cytospin of formalin from small bowel biopsy of a patient with Giardia).



Giardiasis on a duodenal biopsy.

Nomenclature of Giardia species is difficult, as humans and other animals appear to have morphologically identical parasites.

Colonization of the gut results in inflammation and villous atrophy, reducing the gut’s absorptive capability. In humans, infection is symptomatic only about 50% of the time, and protocol for treating asymptomatic individuals is controversial.[4] Symptoms of infection include (in order of frequency) diarrhea, malaise, excessive gas (often flatulence or a foul or sulphuric-tasting belch, which has been known to be so nauseating in taste that it can cause the infected person to vomit), steatorrhoea (pale, foul smelling, greasy stools), epigastric pain, bloating, nausea, diminished interest in food, possible (but rare) vomiting which is often violent, and weight loss.[4] Pus, mucus and blood are occasionally present in the stool. It usually causes “explosive diarrhea” and while unpleasant, is not fatal. In healthy individuals, the condition is usually self-limiting, although the infection can be prolonged in patients who are immunocompromised, or who have decreased gastric acid secretion.[4]

People with recurring Giardia infections, particularly those with a lack of the Immunoglobulin A antibody, may develop chronic disease.

Lactase deficiency may develop in an infection with Giardia, however this usually does not persist for more than a few weeks, and a full recovery is the norm.[citation needed]

Some studies have shown that giardiasis should be considered as a cause of vitamin B12 deficiency, this a result of the problems caused within the intestinal absorption system.[9]


Treatment of drinking water for Giardia is ordinarily indicated in wilderness regions in North America,[10][11] although at least four researchers disagree with this statement, including Robert W. Derlet, a professor at the University of California-Davis School of Medicine, Timothy P. Welch and Thomas R. Welsh of Tulane Medical School and the Children’s Hospital of Cincinnati respectively, and Robert Rockwell, a widely quoted writer who is an engineer by training.[12][13][14][15]

Boiling suspect water for one minute is the surest method to make water safe to drink and kill disease-causing microorganisms like Giardia lamblia if in doubt about whether water is infected with the Giardia parasite.[16]

Treatment and diagnosis

Giardia lamblia infection in humans is frequently misdiagnosed. Accurate diagnosis requires an antigen test or, if that is unavailable, an ova and parasite examination of stool. Multiple stool examinations are recommended, since the cysts and trophozoites are not shed consistently. Given the difficult nature of testing to find the infection, including many false negatives, some patients should be treated on the basis of empirical evidence; treating based on symptoms.[17]

Human infection is conventionally treated with metronidazole, tinidazole or nitazoxanide. Although Metronidazole is the current first-line therapy, it is mutagenic in bacteria and carcinogenic in mice, so should be avoided during pregnancy.[4] It has not directly been linked to causing cancer in humans, only in other mammals, therefore appears safe. One of the most common alternative treatments is berberine sulfate (found in Oregon grape root, goldenseal, yellowroot, and various other plants).[citation needed] Berberine has been shown to have an antimicrobial and an antipyretic effect.[18] Berberine compounds cause uterine stimulation, and so should be avoided in pregnancy. Continuously high dosing of berberine may lead to bradycardia and hypotension in some individuals.[19]


Treatment duration

Possible Side Effects


5–7 days

Metallic taste; nausea; vomiting; dizziness; headache; disulfiram-like effect; neutropenia


Single dose

Metallic taste; nausea; vomiting; belching; dizziness; headache; disulfiram-like effect


3 days

Abdominal pain; diarrhea; vomiting; headache; yellow-green discolouration of urine


5 days

Dizziness; headache; fever; nausea; vomiting; temporary hair loss

Table adapted from Huang, White.[4]

Treatment in animals

Cats can be cured easily, lambs usually simply lose weight, but in calves, the parasites can be fatal and often are not responsive to antibiotics or electrolytes. Carriers among calves can also be asymptomatic. This parasite is deadly for chinchillas, so extra care must be taken by providing them with safe water. Dogs have a high infection rate, as 30% of the population under one year old are known to be infected in kennels. The infection is more prevalent in puppies than in adult dogs. Infected dogs can be isolated and treated, or the entire pack at a kennel can be treated together regardless. Kennels should also be then cleaned with bleach or other cleaning disinfectants. The grass areas used for exercise should be considered contaminated for at least one month after dogs show signs of infection, as cysts can survive in the environment for long periods of time. Prevention can be achieved by quarantine of infected dogs for at least 20 days and careful management and maintenance of a clean water supply.




This picture shows multiple views of a single Giardia lamblia (intestinalis) cyst as imaged at different instrument settings by confocal microscopy.Bar = 10 micrometers.
(A) is the cyst imaged by transmission (differential interference contrast), only.
(B) is the cyst wall selectively imaged through use of fluorescent-labelled (TRITC) antibody that is cyst wall specific.
(C) is the cyst imaged through use of carboxy fluorescein diacetate, a viability stain.
(D) is a composite image of (B) and (C).
(E) is a composite image of (A), (B), and (C).

Under a normal compound light microscope, Giardia often looks like a “clown face,” with two nuclei outlined by adhesive discs above dark median bodies that form the “mouth.” Cysts are oval, have four nuclei, and have clearly visible axostyles. In spite of the common belief that all Eukaryotes have mitochondria, Giardia is one of the few that lack these organelles.


Giardia alternates between two different forms — a hardy, dormant cyst that contaminates water or food and an active, disease-causing form that emerges after the parasite is ingested. National Institute of General Medical Sciences grantee Dr. Frances Gillin of the University of California, San Diego and her colleagues cultivated the entire life cycle of this parasite in the laboratory, and identified biochemical cues in the host’s digestive system which trigger Giardia’s life cycle transformations.[20][21] They also uncovered several ways in which the parasite evades the defences of the infected organism. One of these is by altering the proteins on its surface, which confounds the ability of the infected animal’s immune system to detect and combat the parasite (called antigenic variation). Gillin’s work reveals why Giardia infections are extremely persistent and prone to recur. In addition, these insights into Giardias biology and survival techniques may enable scientists to develop better strategies to understand, prevent, and treat Giardia infections.

In December 2008, Nature published an article showing the discovery of an RNA Interference mechanism that allows Giardia to switch VSPs (Variant-Specific Surface Proteins) to avoid host immune response. The discovery was made by the team working at the Biochemistry and Molecular Biology Laboratory, School of Medicine, Catholic University of Cordoba, Argentina, led by Dr. Hugo Lujan.


Giardia and the other diplomonads are unique in their possession of two nuclei that are similar in appearance, DNA content, transcription and time of replication. There are five chromosomes per the haploid genome The genome has been sequenced and was published in 2007, although the sequence contains several gaps. The sequence is approximately 12 million base pairs and contains approximately 5000 protein coding genes.[22] The GC content is 46%. Trophozoites have a ploidy of four and the ploidy of cysts is eight, which in turn raises the question of how Giardia maintains homogeneity between the chromosomes of the same and opposite nuclei. Modern sequencing technologies have been used to resequence different strains.[23]

Giardia has been assumed to be primitively asexual and with no means of transferring DNA between nuclei. These assumptions make it very difficult to explain the remarkably low level of allelic heterozygosity (< 0.01%) in the genome isolate, WB. However, all these assumptions are now in doubt with the identification of meiotic genes, evidence for recombination among isolates and the evidence for exchange of genetic material between nuclei during the process of encystation.[24]

Seven genotypes have been recognised to date (A-G). Of these B is the most widespread. Only types A and B have been shown to be infectious to humans.


The trophozoite form of Giardia was first observed in 1681 by Antonie van Leeuwenhoek in his own diarrhea stools. The organism was again observed and described in greater detail by Vilém Dušan Lambl in 1859, who thought the organism belonged to the genus Cercomonas and proposed the name Cercomonas intestinalis. His name is still sometimes attached to the genus or the species infecting humans. Thereafter, some have named the genus after him while others have named the species of the human form after him Giardia lamblia. In 1879, Grassi discovered a rodent parasite – now known to be a Giardia species – Dimorphus muris apparently unaware of Lambl’s earlier description. In 1882 and 1883, Johann Künstler described an organism in tadpoles (possibly Giardia agilis) that he named Giardia, this being the first time Giardia was used as a genus name. The genus was chosen to honour Professor Alfred Mathieu Giard of Paris. Raphaël Blanchard, in 1888, proposed the name Lamblia intestinalis,[25] after Lambl. Stiles changed it to Giardia duodenalis in 1902 and to Giardia lamblia in 1915.[26] The same year (1915), Kofoid and Christiansen wrote “The generic name Lamblia Blanchard 1888 should give way to Giardia Kunstler 1882 on ground of priority…”[27] (the epithet being intestinalis) and used Giardia enterica in 1920.[citation needed]

The naming of the species still causes controversy. While initially species names were based on the host of origin leading to over forty species. In 1922 Simon, using morphologic criteria to distinguish between Giardia lamblia and Giardia muris accepted the name Giardia lamblia for the human species. Filice in 1922 further revised the genus when he published a detailed morphologic description of the genus Giardia and proposed that three species names be used on the basis of the morphology of the median body: Giardia agilis, Giardia duodenalis and Giardia muris.[citation needed]

The names for the human parasite Giardia duodenalis, Giardia lamblia and Giardia intestinalis are all in common current use despite the potential for confusion that this has created.[citation needed]

Van Leeuwenhoek’s observations were recreated, using a single lensed microscope of the kind he used, by British microbiologist Brian J. Ford who showed how clearly one could view Giardia through a primitive microscope.[28]

In 1998, a highly publicised Giardia and Cryptosporidium outbreak was reported in Sydney, Australia, but it was found to be due to mis-measurement of the concentrations of microbes in the water supply. A 2004 outbreak in Bergen (Norway) hastened work on adding UV treatment to the water facilities.

In October 2007, Giardia was found in the water supply for parts of Oslo, prompting authorities to advise the public to boil drinking water;[29] but subsequent test showed levels of contamination too low to pose a threat, so this advice has since been cancelled.[30]

In 2008, Giardia was identified as one of the causes of the dysentery afflicting Crusaders in Palestine





Aeromonas Hydrophila

Bacillus Spps

Bacillus Alvei]

Neisseria spps


Klebsiella spps

Escherichia Coli

Salmonella Spps

Vibrio coli

Haemophilus spps

Klebsiella Oxytica

Pteurell ureae

Proteus Spps

Proteus mirabilis

Sreptococcus faecalis

Enterobacter spps

Pateurella Pneumotropica



                                             B.CITRATE TEST



Klebsiella spps

E coli

Enterobactor Spps


Salmonella Spps

Salmonella typhi & paratyphi

Proteus mirabilis

Morganella morganni

Citrobactor freundii

Shigella Spps






                                 C.           coagulase Test



                           S. aureus

S. epidrmidis

  S. delphini

S. Saprophyticus

                           S. hyicus

S. capre

                           S. pseudintermedius


                           S. lutrae


                           S. intermedius




Aspergillosis – the illness caused by various kinds of musty mushrooms of sort Aspergillus. Proceeds with a primary lesion of lungs is more often, streets with immunodeficiencyies accepts serious septic (generalised) flow.

Aetiology. Originators – various kinds of sort Aspergillus. The greatest value in pathology of the human have A. niger, A. flavus, there are also other kinds (A. fumigatus, A. nidulans). Morphologicallies consist of the same mycelium (width 4-6 microns), are sometimes found “heads” with conidiums. At sowing on medium Saburo quickly grow, forming flat colonies, at first white, slightly nappy or velvety, then accept bluish, brown, yellowish and other coloration (depending on a kind); thus their surface becomes farinaceous, powderlike. Aspergillis possess the big biochemical activity, form various enzymes (proteolytic, saccharolytic, lipolytic), and some kinds contain endotoxins at which introduction by an experimental animal paralyses educe and there comes their destruction. Possess allergenic action. From disinfectants on aspergillis solutions of Acidum carbolicum and formalin most activly react.

Epidemiology. Aspergillis eurysynusic in the nature. They can be found in bedrock, grain, a flour, hay (especially mildewed), in a dust of premises where skins are treated, a wool, hemp. Aspergillis even in a dust of medical institutions that caused an intrahospital becoming infected were found. The originator inpours into an organism, as a rule, through air with a dust. From professional bunches workers of agriculture, workers of the weaver’s and textile enterprises are more often amazed. Disease at the relaxed persons can arise and as an endogenous infection contamination as on a mucosa of fauces of healthy humans aspergillis are sometimes found. For last years the aspergillosis at persons with various immunodeficiencyies became an actual problem. In particular, at 20%таких patients mycoses educe, and among the last more than 70 % are necessary on an aspergillosis. Intrahospital infestations of immunodeficient patients by a dust containing aspergillis (air – a dust transmission of infection) are observed. Cases of infestation of the human from sick humans it is not observed.

Pathogenesis. The originator aerogenic by gets on mucosas of the top respiratory tracts. There can come a becoming infected through a skin usually variated by any other pathological process. The leading part in an aspergillosis pathogenesis is played by depression of a host defence of an organism. The aspergillosis complicates various pathological processes of a skin, mucosas, an internals. In particular, pulmonary forms of an aspergillosis arose against a bronchoectatic disease, abscesses of a lung, pulmonary tuberculosis, a cancer of lungs, a chronic bronchitis, etc. last years the aspergillosis began to be observed especially often at persons with immunodeficiencyies (congenital immunodeficiency disorders, the persons receiving antitumoral chemotherapy, immunodepressants, and also a HIV – infected). It meets much more often, than other deep mycoses. At the relaxed persons with a mushroom lungs in the beginning are amazed, then the pleura, lymph nodes are involved in process. Aspergillis can be brought by a blood flow in other organs, forming there specific granulomas which usually abscess. From pulmonary the aspergillosis turns in generalised (septic) and is frequent (over 50 %) comes to an end with destruction of the patient. To salvage it is possible those patients at whom have remained in any measure of function of immune system. At massive inhalation of spores of aspergillis persons with normal immune system can have the acute diffusive pneumonia which is coming to an end with self-recover.

Symptoms and flow. The incubation interval precisely is not established. Aspergillis can amaze any organs and tissues. It is possible to carry following forms to clinical implications:

  1. bronchopulmonary aspergillosis
  2. generalised (septic) aspergillosis
  3. ENT aspergillosis – organs
  4. eye aspergillosis
  5. skin aspergillosis
  6. aspergillosis of bones
  7. other forms of an aspergillosis (a lesion of mucosas of a mouth, genitals, mycotoxicoses and so forth)

Bronchopulmonary aspergillosis can show in the beginning as an aspergillar bronchitis or a tracheobronchitis. In the beginning aspergillis are in blankets of a mucosa of bronchuses, then process extends more deeply, superficial and deeper ulcerations are formed. Disease proceeds chronically, the patient are disturbed by the general delicacy, tussiswith abjection of grey colour of sputum, sometimes with blood streaks. In sputum lumps in which aspergillis contain can be found. Process usually progresses, grasps lungs, the aspergillar pneumonia educe. The pulmonary form of a mycosis can be acute and chronic. At acute forms the body temperature, a fever of usually irregular type raises, repeated cold fits quite often become perceptible, there is a tussis with an abundant viscous mucopurulent or bloody sputum. At some patients the sputum contains zelenovato-grey lumps in which at microscopy clumps of a mycelium and mushroom spores are found. There is a dyspnea, stethalgias, night sweats, delicacy, a weight loss accrues. At auscultation finely bubbly wet rhonchuses, sometimes a pleural rub become perceptible. In blood a leukocytosis (to 20х109/l), the eosinophilia, an ESR is enlarged. At a X-ray inspection inflammatory infiltration in the form of the oval or roundish infiltrates inclined to disintegration is found. Round formed lumens the wide infiltrative shaft is visible.

Chronic forms of a pulmonary aspergillosis are usually secondary and accumulate on various lesions of lungs (bronchiectasias, caverns, abscesses). The clinical picture develops of symptoms of a basic disease and the lesions caused by an aspergillar infection contamination. Sometimes patients note an odour of a mould from a mouth, in sputum there can be the virescent lumps consisting of clumps of a mushroom. Filling of the lumens resulting a basic disease, an original shade in the form of a ball with an air layer between a shade of a ball and lumen sides is characteristic. This layer of gas is taped in the form of an original crescent lumen (“aura”). The lethality at a pulmonary aspergillosis fluctuates from 20 to 37 %.

Septic (generalised) forms of an aspergillosis educe against sharp oppression of immunodefence (sick of AIDS, etc.). This form is characterized by hematogenous diffusion of aspergillis with formation of metastasises in various organs and tissues. Lesions of a gastrointestinal tract (a nausea, vomiting, an odour of a mould from a mouth, the liquid foamy chair containing a considerable quantity of aspergillis), brain abscesses, specific uveites, plural lesions of a skin in the form of original knots can be observed. Changes of a respiratory organs with which usually and the aspergillar sepsis begins are observed also. At sick of AIDS aspergillosis signs are combined with implications of a basic disease and opportunistic infection contaminations (a pneumocystosis, a Kaposi’s sarcoma, cryptosporiodosis, a candidiasis, a generalised herpetic infection contamination, etc.). On this background the aspergillar sepsis, or a generalised aspergillosis, leads to a lethal outcome.

Aspergillosis of ENTs-organs shows in the form of an outside and average otitis, after operations on an intrinsic ear, an aspergillosis with a lesion of a mucosa of a nose and adnexal lumens, a larynx aspergillosis. There can be an aspergillar lesion of a skin and fingernails. The professional aspergillosis can educe at the persons having contact to disputes of various kinds aspergilli (weaving mills, shpagatno-spinning, effecting of malt, etc.). The aspergillosis proceeds at them in the form of a chronic bronchitis, sometimes with bronchospasm symptoms is more often.

Flow of an aspergillosis at sick of AIDS. The aspergillosis is the most frequent mycosis educing against an immunodeficiency. It arises or in the end preAIDS, more often already at the developed clinical semiology of AIDS. The becoming infected comes exogenously air-dust by, that can descend and during stay in medical unit. Disease educes quickly, in the beginning in the form of a pulmonary aspergillosis which then passes in the septic (generalised) form and is accompanied by a lesion of many organs and systems. Proceeds hardly.

Diagnosis and the differential diagnosis. At aspergillosis recognition epidemiological preconditions (a trade, presence of the illnesses relaxing immunodefence, etc.) are considered. From lesions of bronchuses and lungs diagnostic value has long disease, formation of characteristic infiltrates with the subsequent disintegration, character of sputum, a leukocytosis, an eosinophilia. As diagnosis acknowledgement originator abjection (from a sputum, a stuff taken from bronchuses, biopsy samples of the struck organs) serves. From blood aspergillis are excreted was very rarely even at generalised forms of an aspergillosis. Diagnostic value has appearance of antibodies to the originator, taped by means of serological tests. Dermal assays with a specific aspergillar antigen can be used only at it is rather benign a proceeding mycosis at persons with normal immune system. It is necessary to consider, that at a HIV-infected already in a stage preAIDS reactions of hypersensitivity of the slowed down type become negative. On clinical and radiological data the aspergillosis is necessary for differentiating with other mycoses (a nocardiosis, a histoplasmosis, a candidiasis), and also with a pulmonary tuberculosis, abscesses of lungs, neoplasms, a chronic bronchitis.

Treatment. Treatment of a pulmonary and generalised aspergillosis represents a difficult problem. The chemotherapy is a little effective. To therapy of a pulmonary aspergillosis with the circumscribed infiltrate last years successfully apply surgical methods (a lobectomy with a resection of the struck fields of a lung). At the majority of patients operation proceeds without complications and gives good long-term results (relapses it is not observed). At process diffusion on many organs surgical methods are used in a complex with conservative treatment. Prescribe iodine preparations inside in accruing doses. Use potassium Iodidum (or sodium): in the beginning 3 % solution, then 5 and 10 % solution on 1 table spoon 3-4 times a day; 10 % iodine tincture in milk from 3 to 30 drops 3 times a day. From Antimycosis antibiotics Amphotericinum B. A preparation apply intravenously in 5 % glucose solution (50 000 Unit Amphotericinum B in 450 ml of solution of a glucose), introduce driply within 4-6 hours. Daily dose 250 UNITS/KG prescribe from calculation the Preparation introduce 2-3 times a week. Duration of a course depends on the clinical form of an aspergillosis and fluctuates from 4 till 8 weeks (at a HIV-infected more longly). At pulmonary forms of an aspergillosis inhalations of solutions of Sodium iodidum, nystatin of sodium salt (10000 Unit in 1 ml), 0,1 % solution diamond green (5 ml) are shown. At stratification of a consecutive infection (usually staphylococcal) it is possible to apply Oxacillinum (on 1 gramme 4 times a day) or erythromycin (on 0, 25 gramme 4 times a day). Antibiotics of tetracycline bunch and Levomycetinum are contraindicative, as they promote occurrence of aspergillosis. Prescribe vitamins and fortifying treatment.

At treatment of aspergillar lesions of a skin and mucosas use locally antiinflammatory and antimycosis preparations.

The forecast. At pulmonary forms the lethality compounds 20-35 % (at persons with the immunodeficiencyies which have been not bound to a HIV-infection,-nearby 50 %). At the generalised (septic) form the forecast unfavorable. At an aspergillosis of a skin and mucosas the forecast congenial.

Preventive maintenance and actions in the locus. Struggle against a dust and a traumatism on effecting. Wearing of oxygen breathing apparatuses by workers on mills, granaries, vegetable storehouses, the weaver’s enterprises. In medical institutions for persons with immunodeficiencyies it is possible to reduce considerably frequency of an exogenous becoming infected an aspergillosis by clearing of air arriving in chambers by special air filters. For the prevention of secondary (pulmonary) aspergillosis important early recognition and basic disease treatment.


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Jump to: navigation, search



Conidial head of Aspergillus niger

Scientific classification












Micheli, 1729


Several hundred,[1] including:
Aspergillus aculeatus
Aspergillus caesiellus
Aspergillus candidus
Aspergillus carneus
Aspergillus clavatus
Aspergillus deflectus
Aspergillus egyptiacus
Aspergillus fischerianus
Aspergillus flavus
Aspergillus fumigatus
Aspergillus glaucus
Aspergillus nidulans
Aspergillus niger
Aspergillus ochraceus
Aspergillus oryzae
Aspergillus parasiticus
Aspergillus penicilloides
Aspergillus restrictus
Aspergillus sojae
Aspergillus sydowii
Aspergillus tamari
Aspergillus terreus
Aspergillus ustus
Aspergillus versicolor

Aspergillus (IPA: ˌæspərˈdʒɪləs) is a genus consisting of several hundred mold species found in various climates worldwide. Aspergillus was first catalogued in 1729 by the Italian priest and biologist Pier Antonio Micheli. Viewing the fungi under a microscope, Micheli was reminded of the shape of an aspergillum (holy water sprinkler), from Latin spargere (to sprinkle), and named the genus accordingly.[2] Today “aspergillum” is also the name of an asexual spore-forming structure common to all Aspergilli; around one-third of species are also known to have a sexual stage.[1]


Growth and distribution



Aspergillus on a tomato in detail

Aspergillus species are highly aerobic and are found in almost all oxygen-rich environments, where they commonly grow as molds on the surface of a substrate, as a result of the high oxygen tension. Commonly, fungi grow on carbon-rich substrates like monosaccharides (such as glucose) and polysaccharides (such as amylose). Aspergillus species are common contaminants of starchy foods (such as bread and potatoes), and grow in or on many plants and trees.

In addition to growth on carbon sources, many species of Aspergillus demonstrate oligotrophy where they are capable of growing in nutrient-depleted environments, or environments in which there is a complete lack of key nutrients. A. niger is a prime example of this; it can be found growing on damp walls, as a major component of mildew.

Commercial importance



Various Penicillium, Aspergillus spp. (and some other fungi) growing in axenic culture.

Species of Aspergillus are important medically and commercially. Some species can cause infection in humans and other animals. Some infections found in animals have been studied for years. Some species found in animals have been described as new and specific to the investigated disease and others have been known as names already in use for organisms such as saprophytes. More than 60 Aspergillus species are medically relevant pathogens.[3] For humans there are a range of diseases such as infection to the external ear, skin lesions, and ulcers classed as mycetomas.

Other species are important in commercial microbial fermentations. For example, alcoholic beverages such as Japanese sake are often made from rice or other starchy ingredients (like manioc), rather than from grapes or malted barley. Typical microorganisms used to make alcohol, such as yeasts of the genus Saccharomyces, cannot ferment these starches, and so koji mold such as Aspergillus oryzae is used to break down the starches into simpler sugars.

Members of the genus are also sources of natural products that can be used in the development of medications to treat human disease.[4]

Perhaps the largest application of Aspergillus niger is as the major source of citric acid; this organism accounts for over 99% of global citric acid production, or more than 1.4 million tonnes per annum.[citation needed] A. niger is also commonly used for the production of native and foreign enzymes, including glucose oxidase and hen egg white lysozyme. In these instances, the culture is rarely grown on a solid substrate, although this is still common practice in Japan, but is more often grown as a submerged culture in a bioreactor. In this way, the most important parameters can be strictly controlled, and maximal productivity can be achieved. It also makes it far easier to separate the chemical or enzyme of importance from the medium, and is therefore far more cost-effective.


Microalbuminuria (Urine albumin) occurs when the kidney leaks small amounts of albumin into the urine, in other words, when there is an abnormally high permeability for albumin in the renal glomerulus.



The level of albumin protein produced by microalbuminuria can be detected by special albumin-specific urine dipsticks. A microalbumin urine test determines the presence of the albumin in urine. In a properly functioning body, albumin is not normally present in urine because it is retained in the bloodstream by the kidneys.

Microalbuminuria can be diagnosed from a 24-hour urine collection (between 30–300 mg/24 hours) or, more commonly, from elevated concentrations in a spot sample (30 to 300 mg/L). Both must be measured on at least two of three measurements over a two- to three-month period.[1]

An albumin level above the upper limit values is called “macroalbuminuria”, or sometimes just albuminuria. Sometimes, the upper limit value is given as one less (such as 300 being given as 299) to mark that the higher value (here 300) is defined as macroalbuminuria.[2]

To compensate for variations in urine concentration in spot-check samples, it is helpful to compare the amount of albumin in the sample against its concentration of creatinine. This is termed the albumin/creatinine ratio (ACR)[3] and microalbuminuria is defined as ACR ≥3.5 mg/mmol (female) or ≥2.5 mg/mmol(male),[4] or, with both substances measured by mass, as an ACR between 30 and 300 µg albumin/mg creatinine.[5] For the diagnosis of microalbuminuria, care must be taken when collecting sample for the urine ACR. An early morning sample is preferred. The patient should refrain from heavy exercises 24 hours before the test. A repeat test should be done 3 to 6 months after the first positive test for microalbuminuria. Lastly, the test is inaccurate in a person with too much or too little muscle mass. This is due to the variation in creatinine level which is produced by the muscle.[6]

Definitions of microalbuminuria



Lower limit

Upper limit


24h urine collection




mg/24h (milligram albumin per 24 hours)

Short-time urine collection




µg/min (microgram albumin per minute)

Spot urine albumin sample




mg/l (milligram albumin per litre of urine) or
µg/g (microgram albumin per gram of urine)

Spot urine albumin/creatinine ratio



25[8] or 35[8]

mg/mmol (milligram albumin per millimole creatinine)



μg/mg (microgram albumin per milligram creatinine)


2.5[8] or 3.5[8]

25[8] or 35[8]






    *a risk factor for venous thromboembolism

Poliomyelitis In Brief Edited From Wikipedia


From Wikipedia, the free encyclopedia
Jump to: navigation, search
“Polio” redirects here. For the virus, see Poliovirus.
Not to be confused with poliosis, a condition of the hair being or becoming white or grey.
Classification and external resources

A man with an atrophied right leg due to poliomyelitis
ICD-10 A80, B91
ICD-9 045, 138
DiseasesDB 10209
MedlinePlus 001402
eMedicine ped/1843 pmr/6
MeSH C02.182.600.700

Poliomyelitis (pōlee-ō-mī-ə-lītiss), often called polio or infantile paralysis, is an acute, viral, infectious disease spread from person to person, primarily via the fecal-oral route.[1] The term derives from the Greek poliós (πολιός), meaning “grey”, myelós (µυελός “marrow”), referring to the grey matter of the spinal cord, and the suffix -itis, which denotes inflammation.,[2] i.e., inflammation of the spinal cord’s grey matter, although a severe infection can extend into the brainstem and even higher structures, resulting in polioencephalitis, producing apnea that requires mechanical assistance such as an iron lung.

Although approximately 90% of polio infections cause no symptoms at all, affected individuals can exhibit a range of symptoms if the virus enters the blood stream.[3] In about 1% of cases, the virus enters the central nervous system, preferentially infecting and destroying motor neurons, leading to muscle weakness and acute flaccid paralysis. Different types of paralysis may occur, depending on the nerves involved. Spinal polio is the most common form, characterized by asymmetric paralysis that most often involves the legs. Bulbar polio leads to weakness of muscles innervated by cranial nerves. Bulbospinal polio is a combination of bulbar and spinal paralysis.[4]

Poliomyelitis was first recognized as a distinct condition by Jakob Heine in 1840.[5] Its causative agent, poliovirus, was identified in 1908 by Karl Landsteiner.[5] Although major polio epidemics were unknown before the late 19th century, polio was one of the most dreaded childhood diseases of the 20th century. Polio epidemics have crippled thousands of people, mostly young children; the disease has caused paralysis and death for much of human history. Polio had existed for thousands of years quietly as an endemic pathogen until the 1880s, when major epidemics began to occur in Europe; soon after, widespread epidemics appeared in the United States.[6]

By 1910, much of the world experienced a dramatic increase in polio cases and epidemics became regular events, primarily in cities during the summer months. These epidemics — which left thousands of children and adults paralyzed — provided the impetus for a “Great Race” towards the development of a vaccine. Developed in the 1950s, polio vaccines have reduced the global number of polio cases per year from many hundreds of thousands to under a thousand today.[7] Enhanced vaccination efforts led by Rotary International, the World Health Organization, and UNICEF should result in global eradication of the disease.[8][9]


Outcomes of poliovirus infection
Outcome Proportion of cases[4]
Asymptomatic 90–95%
Minor illness 4–8%
Nonparalytic aseptic
Paralytic poliomyelitis 0.1–0.5%
— Spinal polio 79% of paralytic cases
— Bulbospinal polio 19% of paralytic cases
— Bulbar polio 2% of paralytic cases

The term “poliomyelitis” is used to identify the disease caused by any of the three serotypes of poliovirus. Two basic patterns of polio infection are described: a minor illness which does not involve the central nervous system (CNS), sometimes called abortive poliomyelitis, and a major illness involving the CNS, which may be paralytic or nonparalytic.[10] In most people with a normal immune system, a poliovirus infection is asymptomatic. Rarely, the infection produces minor symptoms; these may include upper respiratory tract infection (sore throat and fever), gastrointestinal disturbances (nausea, vomiting, abdominal pain, constipation or, rarely, diarrhea), and influenza-like illness.[4]

The virus enters the central nervous system in about 3% of infections. Most patients with CNS involvement develop nonparalytic aseptic meningitis, with symptoms of headache, neck, back, abdominal and extremity pain, fever, vomiting, lethargy, and irritability.[2][11] About one to five in 1000 cases progress to paralytic disease, in which the muscles become weak, floppy and poorly controlled, and, finally, completely paralyzed; this condition is known as acute flaccid paralysis.[12] Depending on the site of paralysis, paralytic poliomyelitis is classified as spinal, bulbar, or bulbospinal. Encephalitis, an infection of the brain tissue itself, can occur in rare cases, and is usually restricted to infants. It is characterized by confusion, changes in mental status, headaches, fever, and, less commonly, seizures and spastic paralysis.[13]


Main article: Poliovirus

A TEM micrograph of poliovirus

Poliomyelitis is caused by infection with a member of the genus Enterovirus known as poliovirus (PV). This group of RNA viruses colonize the gastrointestinal tract[1] — specifically the oropharynx and the intestine. The incubation time (to the first signs and symptoms) ranges from three to 35 days, with a more common span of six to 20 days.[4] PV infects and causes disease in humans alone.[3] Its structure is very simple, composed of a single (+) sense RNA genome enclosed in a protein shell called a capsid.[3] In addition to protecting the virus’s genetic material, the capsid proteins enable poliovirus to infect certain types of cells. Three serotypes of poliovirus have been identified—poliovirus type 1 (PV1), type 2 (PV2), and type 3 (PV3)—each with a slightly different capsid protein.[14] All three are extremely virulent and produce the same disease symptoms.[3] PV1 is the most commonly encountered form, and the one most closely associated with paralysis.[15]

Individuals who are exposed to the virus, either through infection or by immunization with polio vaccine, develop immunity. In immune individuals, IgA antibodies against poliovirus are present in the tonsils and gastrointestinal tract, and are able to block virus replication; IgG and IgM antibodies against PV can prevent the spread of the virus to motor neurons of the central nervous system.[16] Infection or vaccination with one serotype of poliovirus does not provide immunity against the other serotypes, and full immunity requires exposure to each serotype.[16]

A rare condition with a similar presentation, nonpoliovirus poliomyelitis, may result from infections with nonpoliovirus enteroviruses.[17]


Poliomyelitis is highly contagious via the oral-oral (oropharyngeal source) and fecal-oral (intestinal source) routes.[16] In endemic areas, wild polioviruses can infect virtually the entire human population.[18] It is seasonal in temperate climates, with peak transmission occurring in summer and autumn.[16] These seasonal differences are far less pronounced in tropical areas.[18] The time between first exposure and first symptoms, known as the incubation period, is usually six to 20 days, with a maximum range of three to 35 days.[19] Virus particles are excreted in the feces for several weeks following initial infection.[19] The disease is transmitted primarily via the fecal-oral route, by ingesting contaminated food or water. It is occasionally transmitted via the oral-oral route,[15] a mode especially visible in areas with good sanitation and hygiene.[16] Polio is most infectious between seven and 10 days before and after the appearance of symptoms, but transmission is possible as long as the virus remains in the saliva or feces.[15]

Factors that increase the risk of polio infection or affect the severity of the disease include immune deficiency,[20] malnutrition,[21] tonsillectomy,[22] physical activity immediately following the onset of paralysis,[23] skeletal muscle injury due to injection of vaccines or therapeutic agents,[24] and pregnancy.[25] Although the virus can cross the placenta during pregnancy, the fetus does not appear to be affected by either maternal infection or polio vaccination.[26] Maternal antibodies also cross the placenta, providing passive immunity that protects the infant from polio infection during the first few months of life.[27]

As a precaution against infection, public swimming pools were often closed in affected areas during poliomyelitis epidemics.


A blockage of the lumbar anterior spinal cord artery due to polio (PV3)

Poliovirus enters the body through the mouth, infecting the first cells with which it comes in contact — the pharynx and intestinal mucosa. It gains entry by binding to an immunoglobulin-like receptor, known as the poliovirus receptor or CD155, on the cell membrane.[28] The virus then hijacks the host cell’s own machinery, and begins to replicate. Poliovirus divides within gastrointestinal cells for about a week, from where it spreads to the tonsils (specifically the follicular dendritic cells residing within the tonsilar germinal centers), the intestinal lymphoid tissue including the M cells of Peyer’s patches, and the deep cervical and mesenteric lymph nodes, where it multiplies abundantly. The virus is subsequently absorbed into the bloodstream.[29]

Known as viremia, the presence of virus in the bloodstream enables it to be widely distributed throughout the body. Poliovirus can survive and multiply within the blood and lymphatics for long periods of time, sometimes as long as 17 weeks.[30] In a small percentage of cases, it can spread and replicate in other sites, such as brown fat, the reticuloendothelial tissues, and muscle.[31] This sustained replication causes a major viremia, and leads to the development of minor influenza-like symptoms. Rarely, this may progress and the virus may invade the central nervous system, provoking a local inflammatory response. In most cases, this causes a self-limiting inflammation of the meninges, the layers of tissue surrounding the brain, which is known as nonparalytic aseptic meningitis.[2] Penetration of the CNS provides no known benefit to the virus, and is quite possibly an incidental deviation of a normal gastrointestinal infection.[32] The mechanisms by which poliovirus spreads to the CNS are poorly understood, but it appears to be primarily a chance event—largely independent of the age, gender, or socioeconomic position of the individual.[32]

Paralytic polio

Denervation of skeletal muscle tissue secondary to poliovirus infection can lead to paralysis.

In around 1% of infections, poliovirus spreads along certain nerve fiber pathways, preferentially replicating in and destroying motor neurons within the spinal cord, brain stem, or motor cortex. This leads to the development of paralytic poliomyelitis, the various forms of which (spinal, bulbar, and bulbospinal) vary only with the amount of neuronal damage and inflammation that occurs, and the region of the CNS affected.

The destruction of neuronal cells produces lesions within the spinal ganglia; these may also occur in the reticular formation, vestibular nuclei, cerebellar vermis, and deep cerebellar nuclei.[32] Inflammation associated with nerve cell destruction often alters the color and appearance of the gray matter in the spinal column, causing it to appear reddish and swollen.[2] Other destructive changes associated with paralytic disease occur in the forebrain region, specifically the hypothalamus and thalamus.[32] The molecular mechanisms by which poliovirus causes paralytic disease are poorly understood.

Early symptoms of paralytic polio include high fever, headache, stiffness in the back and neck, asymmetrical weakness of various muscles, sensitivity to touch, difficulty swallowing, muscle pain, loss of superficial and deep reflexes, paresthesia (pins and needles), irritability, constipation, or difficulty urinating. Paralysis generally develops one to ten days after early symptoms begin, progresses for two to three days, and is usually complete by the time the fever breaks.[33]

The likelihood of developing paralytic polio increases with age, as does the extent of paralysis. In children, nonparalytic meningitis is the most likely consequence of CNS involvement, and paralysis occurs in only one in 1000 cases. In adults, paralysis occurs in one in 75 cases.[34] In children under five years of age, paralysis of one leg is most common; in adults, extensive paralysis of the chest and abdomen also affecting all four limbs — quadriplegia — is more likely.[35] Paralysis rates also vary depending on the serotype of the infecting poliovirus; the highest rates of paralysis (one in 200) are associated with poliovirus type 1, the lowest rates (one in 2,000) are associated with type 2.[36]

Spinal polio

The location of motor neurons in the anterior horn cells of the spinal column

Spinal polio, the most common form of paralytic poliomyelitis, results from viral invasion of the motor neurons of the anterior horn cells, or the ventral (front) grey matter section in the spinal column, which are responsible for movement of the muscles, including those of the trunk, limbs, and the intercostal muscles.[12] Virus invasion causes inflammation of the nerve cells, leading to damage or destruction of motor neuron ganglia. When spinal neurons die, Wallerian degeneration takes place, leading to weakness of those muscles formerly innervated by the now-dead neurons.[37] With the destruction of nerve cells, the muscles no longer receive signals from the brain or spinal cord; without nerve stimulation, the muscles atrophy, becoming weak, floppy and poorly controlled, and finally completely paralyzed.[12] Progression to maximum paralysis is rapid (two to four days), and is usually associated with fever and muscle pain.[37] Deep tendon reflexes are also affected, and are usually absent or diminished; sensation (the ability to feel) in the paralyzed limbs, however, is not affected.[37]

The extent of spinal paralysis depends on the region of the cord affected, which may be cervical, thoracic, or lumbar.[38] The virus may affect muscles on both sides of the body, but more often the paralysis is asymmetrical.[29] Any limb or combination of limbs may be affected—one leg, one arm, or both legs and both arms. Paralysis is often more severe proximally (where the limb joins the body) than distally (the fingertips and toes).[29]

Bulbar polio

The location and anatomy of the bulbar region (in orange)

Making up about 2% of cases of paralytic polio, bulbar polio occurs when poliovirus invades and destroys nerves within the bulbar region of the brain stem.[4] The bulbar region is a white matter pathway that connects the cerebral cortex to the brain stem. The destruction of these nerves weakens the muscles supplied by the cranial nerves, producing symptoms of encephalitis, and causes difficulty breathing, speaking and swallowing.[11] Critical nerves affected are the glossopharyngeal nerve (which partially controls swallowing and functions in the throat, tongue movement, and taste), the vagus nerve (which sends signals to the heart, intestines, and lungs), and the accessory nerve (which controls upper neck movement). Due to the effect on swallowing, secretions of mucus may build up in the airway, causing suffocation.[33] Other signs and symptoms include facial weakness (caused by destruction of the trigeminal nerve and facial nerve, which innervate the cheeks, tear ducts, gums, and muscles of the face, among other structures), double vision, difficulty in chewing, and abnormal respiratory rate, depth, and rhythm (which may lead to respiratory arrest). Pulmonary edema and shock are also possible and may be fatal.[38]

Bulbospinal polio

Approximately 19% of all paralytic polio cases have both bulbar and spinal symptoms; this subtype is called respiratory or bulbospinal polio.[4] Here, the virus affects the upper part of the cervical spinal cord (cervical vertebrae C3 through C5), and paralysis of the diaphragm occurs. The critical nerves affected are the phrenic nerve (which drives the diaphragm to inflate the lungs) and those that drive the muscles needed for swallowing. By destroying these nerves, this form of polio affects breathing, making it difficult or impossible for the patient to breathe without the support of a ventilator. It can lead to paralysis of the arms and legs and may also affect swallowing and heart functions.[39]


Paralytic poliomyelitis may be clinically suspected in individuals experiencing acute onset of flaccid paralysis in one or more limbs with decreased or absent tendon reflexes in the affected limbs that cannot be attributed to another apparent cause, and without sensory or cognitive loss.[40]

A laboratory diagnosis is usually made based on recovery of poliovirus from a stool sample or a swab of the pharynx. Antibodies to poliovirus can be diagnostic, and are generally detected in the blood of infected patients early in the course of infection.[4] Analysis of the patient’s cerebrospinal fluid (CSF), which is collected by a lumbar puncture (“spinal tap”), reveals an increased number of white blood cells (primarily lymphocytes) and a mildly elevated protein level. Detection of virus in the CSF is diagnostic of paralytic polio, but rarely occurs.[4]

If poliovirus is isolated from a patient experiencing acute flaccid paralysis, it is further tested through oligonucleotide mapping (genetic fingerprinting), or more recently by PCR amplification, to determine whether it is “wild type” (that is, the virus encountered in nature) or “vaccine type” (derived from a strain of poliovirus used to produce polio vaccine).[41] It is important to determine the source of the virus because for each reported case of paralytic polio caused by wild poliovirus, an estimated another 200 to 3,000 contagious asymptomatic carriers exist.[42]


Passive immunization

In 1950, William Hammon at the University of Pittsburgh purified the gamma globulin component of the blood plasma of polio survivors.[43] Hammon proposed the gamma globulin, which contained antibodies to poliovirus, could be used to halt poliovirus infection, prevent disease, and reduce the severity of disease in other patients who had contracted polio. The results of a large clinical trial were promising; the gamma globulin was shown to be about 80% effective in preventing the development of paralytic poliomyelitis.[44] It was also shown to reduce the severity of the disease in patients who developed polio.[43] The gamma globulin approach was later deemed impractical for widespread use, however, due in large part to the limited supply of blood plasma, so the medical community turned its focus to the development of a polio vaccine.[45]


Main article: Polio vaccine

A child receiving an oral polio vaccine

Two types of vaccine are used throughout the world to combat polio. Both types induce immunity to polio, efficiently blocking person-to-person transmission of wild poliovirus, thereby protecting both individual vaccine recipients and the wider community (so-called herd immunity).[46]

The first candidate polio vaccine, based on one serotype of a live but attenuated (weakened) virus, was developed by the virologist Hilary Koprowski. Koprowski’s prototype vaccine was given to an eight-year-old boy on February 27, 1950.[47] Koprowski continued to work on the vaccine throughout the 1950s, leading to large-scale trials in the then Belgian Congo and the vaccination of seven million children in Poland against serotypes PV1 and PV3 between 1958 and 1960.[48]

The second inactivated virus vaccine was developed in 1952 by Jonas Salk at the University of Pittsburgh, and announced to the world on April 12, 1955.[49] The Salk vaccine, or inactivated poliovirus vaccine (IPV), is based on poliovirus grown in a type of monkey kidney tissue culture (vero cell line), which is chemically inactivated with formalin.[16] After two doses of IPV (given by injection), 90% or more of individuals develop protective antibody to all three serotypes of poliovirus, and at least 99% are immune to poliovirus following three doses.[4]

Subsequently, Albert Sabin developed another live, oral polio vaccine (OPV). It was produced by the repeated passage of the virus through nonhuman cells at subphysiological temperatures.[50] The attenuated poliovirus in the Sabin vaccine replicates very efficiently in the gut, the primary site of wild poliovirus infection and replication, but the vaccine strain is unable to replicate efficiently within nervous system tissue.[51] A single dose of Sabin’s oral polio vaccine produces immunity to all three poliovirus serotypes in about 50% of recipients. Three doses of live-attenuated OPV produce protective antibody to all three poliovirus types in more than 95% of recipients.[4] Human trials of Sabin’s vaccine began in 1957,[52] and in 1958 it was selected, in competition with the live vaccines of Koprowski and other researchers, by the US National Institutes of Health.[48] Licensed in 1962,[52] it rapidly became the only polio vaccine used worldwide.[48]

Because OPV is inexpensive, easy to administer, and produces excellent immunity in the intestine (which helps prevent infection with wild virus in areas where it is endemic), it has been the vaccine of choice for controlling poliomyelitis in many countries.[53] On very rare occasions (about one case per 750,000 vaccine recipients), the attenuated virus in OPV reverts into a form that can paralyze.[19] Most industrialized countries have switched to IPV, which cannot revert, either as the sole vaccine against poliomyelitis or in combination with oral polio vaccine.[54]


There is no cure for polio. The focus of modern treatment has been on providing relief of symptoms, speeding recovery and preventing complications. Supportive measures include antibiotics to prevent infections in weakened muscles, analgesics for pain, moderate exercise and a nutritious diet.[55] Treatment of polio often requires long-term rehabilitation, including occupational therapy, physical therapy, braces, corrective shoes and, in some cases, orthopedic surgery.[38]

Portable ventilators may be required to support breathing. Historically, a noninvasive, negative-pressure ventilator, more commonly called an iron lung, was used to artificially maintain respiration during an acute polio infection until a person could breathe independently (generally about one to two weeks). Today, many polio survivors with permanent respiratory paralysis use modern jacket-type negative-pressure ventilators worn over the chest and abdomen.[56]

Other historical treatments for polio include hydrotherapy, electrotherapy, massage and passive motion exercises, and surgical treatments, such as tendon lengthening and nerve grafting.[12] Devices such as rigid braces and body casts—which tended to cause muscle atrophy due to the limited movement of the user—were also touted as effective treatments.[57]


Patients with abortive polio infections recover completely. In those who develop only aseptic meningitis, the symptoms can be expected to persist for two to ten days, followed by complete recovery.[58] In cases of spinal polio, if the affected nerve cells are completely destroyed, paralysis will be permanent; cells that are not destroyed, but lose function temporarily, may recover within four to six weeks after onset.[58] Half the patients with spinal polio recover fully; one-quarter recover with mild disability, and the remaining quarter are left with severe disability.[59] The degree of both acute paralysis and residual paralysis is likely to be proportional to the degree of viremia, and inversely proportional to the degree of immunity.[32] Spinal polio is rarely fatal.[33]

A child with a deformity of her right leg due to polio

Without respiratory support, consequences of poliomyelitis with respiratory involvement include suffocation or pneumonia from aspiration of secretions.[56] Overall, 5–10% of patients with paralytic polio die due to the paralysis of muscles used for breathing. The mortality rate varies by age: 2–5% of children and up to 15–30% of adults die.[4] Bulbar polio often causes death if respiratory support is not provided;[39] with support, its mortality rate ranges from 25 to 75%, depending on the age of the patient.[4][60] When positive pressure ventilators are available, the mortality can be reduced to 15%.[61]


Many cases of poliomyelitis result in only temporary paralysis.[12] Nerve impulses return to the formerly paralyzed muscle within a month, and recovery is usually complete in six to eight months.[58] The neurophysiological processes involved in recovery following acute paralytic poliomyelitis are quite effective; muscles are able to retain normal strength even if half the original motor neurons have been lost.[62] Paralysis remaining after one year is likely to be permanent, although modest recoveries of muscle strength are possible 12 to 18 months after infection.[58]

One mechanism involved in recovery is nerve terminal sprouting, in which remaining brainstem and spinal cord motor neurons develop new branches, or axonal sprouts.[63] These sprouts can reinnervate orphaned muscle fibers that have been denervated by acute polio infection,[64] restoring the fibers’ capacity to contract and improving strength.[65] Terminal sprouting may generate a few significantly enlarged motor neurons doing work previously performed by as many as four or five units:[34] a single motor neuron that once controlled 200 muscle cells might control 800 to 1000 cells. Other mechanisms that occur during the rehabilitation phase, and contribute to muscle strength restoration, include myofiber hypertrophy—enlargement of muscle fibers through exercise and activity—and transformation of type II muscle fibers to type I muscle fibers.[64][66]

In addition to these physiological processes, the body possesses a number of compensatory mechanisms to maintain function in the presence of residual paralysis. These include the use of weaker muscles at a higher than usual intensity relative to the muscle’s maximal capacity, enhancing athletic development of previously little-used muscles, and using ligaments for stability, which enables greater mobility.[66]


Residual complications of paralytic polio often occur following the initial recovery process.[11] Muscle paresis and paralysis can sometimes result in skeletal deformities, tightening of the joints and movement disability. Once the muscles in the limb become flaccid, they may interfere with the function of other muscles. A typical manifestation of this problem is equinus foot (similar to club foot). This deformity develops when the muscles that pull the toes downward are working, but those that pull it upward are not, and the foot naturally tends to drop toward the ground. If the problem is left untreated, the Achilles tendons at the back of the foot retract and the foot cannot take on a normal position. Polio victims that develop equinus foot cannot walk properly because they cannot put their heel on the ground. A similar situation can develop if the arms become paralyzed.[67] In some cases the growth of an affected leg is slowed by polio, while the other leg continues to grow normally. The result is that one leg is shorter than the other and the person limps and leans to one side, in turn leading to deformities of the spine (such as scoliosis).[67] Osteoporosis and increased likelihood of bone fractures may occur. An intervention to prevent or lessen length disparity can be to perform an epiphysiodesis on the distal femoral and proximal tibial/fibular condyles, so that limb’s growth is artificially stunted, and by the time of epiphyseal (growth) plate closure, the legs are more equal in length. Other surgery to re-balance muscular agonist/antagonist imbalances may also be helpful. Extended use of braces or wheelchairs may cause compression neuropathy, as well as a loss of proper function of the veins in the legs, due to pooling of blood in paralyzed lower limbs.[39][68] Complications from prolonged immobility involving the lungs, kidneys and heart include pulmonary edema, aspiration pneumonia, urinary tract infections, kidney stones, paralytic ileus, myocarditis and cor pulmonale.[39][68]

Post-polio syndrome

Main article: Post-polio syndrome

Between 25% and 50% of individuals who survive paralytic polio in childhood develop additional symptoms decades after recovering from the acute infection,[69] notably new muscle weakness and extreme fatigue. This condition is known as post-polio syndrome (PPS) or post-polio sequelae.[70] The symptoms of PPS are thought to involve a failure of the over-sized motor units created during recovery from paralytic disease.[71][72] Factors that increase the risk of PPS include the length of time since acute poliovirus infection, the presence of permanent residual impairment after recovery from the acute illness, and both overuse and disuse of neurons.[70] Post-polio syndrome is not an infectious process, and persons experiencing the syndrome do not shed poliovirus.[4]


Disability-adjusted life year for poliomyelitis per 100,000 inhabitants in 2004.

  no data

While now rare in the Western world, polio is still endemic to South Asia, particularly Pakistan, and Nigeria. Following the widespread use of poliovirus vaccine in the mid-1950s, the incidence of poliomyelitis declined dramatically in many industrialized countries. A global effort to eradicate polio began in 1988, led by the World Health Organization, UNICEF, and The Rotary Foundation.[73] These efforts have reduced the number of annual diagnosed cases by 99%; from an estimated 350,000 cases in 1988 to a low of 483 cases in 2001, after which it has remained at a level of about 1,000 cases per year (1,606 in 2009).[74][75][76] Polio is one of only two diseases currently the subject of a global eradication program, the other being Guinea worm disease. So far, the only diseases completely eradicated by humankind are smallpox, which happened in 1979,[77] and rinderpest in 2010.[78] A number of eradication milestones have already been reached, and several regions of the world have been certified polio-free. The Americas were declared polio-free in 1994.[79] In 2000 polio was officially eliminated in 36 Western Pacific countries, including China and Australia.[80][81] Europe was declared polio-free in 2002.[82] As of 2012, polio remains endemic in only three countries: Nigeria, Pakistan, and Afghanistan,[74][83] although it continues to cause epidemics in other nearby countries due to hidden or reestablished transmission.[84] For example, despite eradication ten years prior, an outbreak was confirmed in China in September 2011 involving a strain prevalent in neighboring Pakistan.[85] Since January 2011, there were no reported cases of the disease in India, and hence in February 2012, the country was taken off the WHO list of polio endemic countries. It is reported that if there are no cases of polio in the country for two more years, it will be declared as a polio-free country.[86][87]

Christopher Hitchens wrote that he learned in 2005 that in Northern Nigeria—a country which at that time was considered provisionally polio free—an Islamic Fatwah was issued declaring that the polio vaccine was a conspiracy by the United States and the United Nations against the Muslim faith, saying that the drops were designed to sterilize the true believers. Subsequently, polio reappeared in Nigeria and spread from there to several other countries.[88]


An Egyptian stele thought to represent a polio victim, 18th Dynasty (1403–1365 BC)

The effects of polio have been known since prehistory; Egyptian paintings and carvings depict otherwise healthy people with withered limbs, and children walking with canes at a young age.[5] The first clinical description was provided by the English physician Michael Underwood in 1789, where he refers to polio as “a debility of the lower extremities”.[89] The work of physicians Jakob Heine in 1840 and Karl Oskar Medin in 1890 led to it being known as Heine-Medin disease.[90] The disease was later called infantile paralysis, based on its propensity to affect children.

Before the 20th century, polio infections were rarely seen in infants before six months of age, most cases occurring in children six months to four years of age.[91] Poorer sanitation of the time resulted in a constant exposure to the virus, which enhanced a natural immunity within the population. In developed countries during the late 19th and early 20th centuries, improvements were made in community sanitation, including better sewage disposal and clean water supplies. These changes drastically increased the proportion of children and adults at risk of paralytic polio infection, by reducing childhood exposure and immunity to the disease.[91]

Small localized paralytic polio epidemics began to appear in Europe and the United States around 1900.[6] Outbreaks reached pandemic proportions in Europe, North America, Australia, and New Zealand during the first half of the 20th century. By 1950 the peak age incidence of paralytic poliomyelitis in the United States had shifted from infants to children aged five to nine years, when the risk of paralysis is greater; about one-third of the cases were reported in persons over 15 years of age.[92] Accordingly, the rate of paralysis and death due to polio infection also increased during this time.[6] In the United States, the 1952 polio epidemic became the worst outbreak in the nation’s history. Of nearly 58,000 cases reported that year 3,145 died and 21,269 were left with mild to disabling paralysis.[93] Intensive care medicine has its origin in the fight against polio.[94] Most hospitals in the 1950s had limited access to iron lungs for patients unable to breathe without mechanical assistance. Respiratory centers designed to assist the most severe polio patients, first established in 1952 at the Blegdam Hospital of Copenhagen by Danish anesthesiologist Bjørn Ibsen, were the harbingers of subsequent intensive care units (ICU). (A year later, Ibsen would establish the world’s first dedicated ICU.)[95]

The polio epidemics changed not only the lives of those who survived them, but also affected profound cultural changes; spurring grassroots fund-raising campaigns that would revolutionize medical philanthropy, and give rise to the modern field of rehabilitation therapy. As one of the largest disabled groups in the world, polio survivors also helped to advance the modern disability rights movement through campaigns for the social and civil rights of the disabled. The World Health Organization estimates that there are 10 to 20 million polio survivors worldwide.[96] In 1977 there were 254,000 persons living in the United States who had been paralyzed by polio.[97] According to doctors and local polio support groups, some 40,000 polio survivors with varying degrees of paralysis live in Germany, 30,000 in Japan, 24,000 in France, 16,000 in Australia, 12,000 in Canada and 12,000 in the United Kingdom.[96] Many notable individuals have survived polio and often credit the prolonged immobility and residual paralysis associated with polio as a driving force in their lives and careers.[98]

The disease was very well publicized during the polio epidemics of the 1950s, with extensive media coverage of any scientific advancements that might lead to a cure. Thus, the scientists working on polio became some of the most famous of the century. Fifteen scientists and two laymen who made important contributions to the knowledge and treatment of poliomyelitis are honored by the Polio Hall of Fame, which was dedicated in 1957 at the Roosevelt Warm Springs Institute for Rehabilitation in Warm Springs, Georgia, US. In 2008 four organizations (Rotary International, the World Health Organization, the U.S. Centers for Disease Control and UNICEF) were added to the Hall of Fame.[99][100]

Poliomyelitis : A Severe Viral Infection


WHO/B. Kadirov

Poliomyelitis (polio) is a highly infectious viral disease, which mainly affects young children. The virus is transmitted through contaminated food and water, and multiplies in the intestine, from where it can invade the nervous system. Many infected people have no symptoms, but do excrete the virus in their faeces, hence transmitting infection to others.

Initial symptoms of polio include fever, fatigue, headache, vomiting, stiffness in the neck, and pain in the limbs. In a small proportion of cases, the disease causes paralysis, which is often permanent. Polio can only be prevented by immunization.


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