The term childhood disease is sometimes subjective, and does not refer to an accepted, categorical list. Nearly all the diseases in this list can also be contracted by adults, and, of course, all children can contract diseases not categorized as "childhood diseases".
Some childhood diseases include:
* Candidiasis ("Thrush")
* Chicken pox
* Chagas disease
* Croup
* Cytomegalovirus (the virus most frequently transmitted before birth)
* Duchenne muscular dystrophy
* Measles
* Mumps
* Rheumatic fever
* Rubella
* Whooping cough
* fifth disease
CANDIDIASISCandidiasis, commonly called yeast infection or thrush, is a fungal infection of any of the Candida species, of which Candida albicans is probably the most common.
LocationsIn immunocompetent people, candidiasis can usually only be found in exposed and moist parts of the body, such as:
* the oral cavity (oral thrush)
* the vagina (vaginal candidiasis or thrush)
* folds of skin in the diaper area (diaper rash)
* the most common cause of vaginal irritation or vaginitis
* can also occur on the male genitals, particularly in uncircumcised men.
In immunocompromised patients, the Candida infection can become systemic, causing a much more serious condition, fungemia.
CausesYeast organisms are always present in all people, but are usually prevented from "overgrowth" (uncontrolled multiplication resulting in symptoms) by naturally occurring microorganisms.
At least three quarters of all women will experience candidiasis at some point in their lives. The Candida albicans organism is found in the vaginas of almost all women and normally causes no problems. However, when it gets out of balance with the other "normal flora," such as lactobacilli (which can also be harmed by using douches), an overgrowth and symptoms can result. Pregnancy, the use of oral contraceptives and some antibiotics, and diabetes mellitus increase the risk of infection.
SymptomsThe most common symptoms are itching and irritation of the vagina and/or vulva. A whitish or whitish-gray discharge may be present, sometimes resembling cottage cheese, and may have a "yeasty" smell like beer or baking bread. Many women mistake the symptoms of the more common bacterial vaginosis for a yeast infection. In a 2002 study published in the Journal of Obstetrics and Gynecology, only 33 percent of women who were self treating for a yeast infection actually had a yeast infection. Instead they had either bacterial vaginosis or a mixed-type infection. Currently, bacterial vaginosis can only be diagnosed during a doctor's visit.
DiagnosisKOH (potassium hydroxide) preparation can be diagnostic. A scraping or swab of the affected area is placed on a microscope slide. A single drop of 10% solution of KOH is then placed on the slide. The KOH dissolves the skin cells but leaves the Candida untouched. When viewed under a microscope the hyphae and pseudo spores of Candida are visible. Their presence in large numbers strongly suggest a yeast infection.
Swab and culture is performed by rubbing a sterile swab on the infected skin surface. The swab is then rubbed across a culture medium. The medium is incubated for several days, during which time colonies of yeast and or bacteria develop. The characteristics of the colonies provide a presumptive diagnosis of the organism.
TreatmentCandidiasis is alleged to be successfully treated either with home remedies or, in the case of a more severe infection, with either over the counter or prescription antifungal medications. Home remedies for candidiasis include the consumption or direct application of yogurt, which contains lactobacillus (probiotics, "friendly" bacteria that kill yeast), acidophilus tablets or salves, and even lightly crushed cloves of garlic, which yield allicin, an antifungal. Boric acid has also been used to treat yeast infections when gelcaps are filled with boric acid powder and two are inserted at bedtime for three to four nights.
While home remedies can offer relief in minor cases of infection, seeking medical attention can be necessary because the extent of the infection sometimes cannot be judged well by the sufferer. Prescription medication is often the only solution to an infection; the antifungal drugs commonly used to treat candidiasis are topical clotrimazole, topical nystatin, fluconazole, topical ketoconazole. In severe infections (generally in hospitalized patients), amphotericin B, caspofungin, or voriconazole may be used. These medications are not effective against the more common bacterial vaginosis.
If indicated, an underlying reason should be looked for. As an example, oral candidiasis is often linked to the use of inhaled steroids in asthma medication. Patients on long term inhaled steroids should rinse their mouth after each dose of steroids. It can also be the first sign of a more serious condition, such as HIV. Babies with diaper rash should have their diaper areas kept clean, dry, and exposed to air as much as possible. Sugar assists the overgrowth of yeast; thus, the increased prevalence of yeast infections in patients with diabetes mellitus, as noted above. In the case of frequent yeast infections, sugar can be looked to as a culprit and should be avoided. Nutritionists often recommend avoidance diets, eliminating sugar and often many other foods for a period. Extensive antibiotic treatment is sometimes implicated, and probiotics are then recommended.
Following the health tips at vulvovaginal health can help prevent vaginal candidiasis. Local treatment may include vaginal suppositories or medicated douches.
CHICKENPOXChickenpox, also spelled chicken pox, is the common name for Varicella simplex, classically one of the childhood infectious diseases caught and survived by most children.
Chickenpox is caused by the varicella-zoster virus (VZV), also known as human herpes virus 3 (HHV-3), one of the eight herpes viruses known to affect humans. It starts with conjunctival and catarrhal symptoms, moderate fever and then characteristic spots appearing in two or three waves, mainly on the body and head rather than the hands and becoming itchy raw pox (pocks), small open sores which heal mostly without scarring.
EffectsChickenpox has a two-week incubation period and is highly contagious by air transmission two days before symptoms appear. Therefore, chickenpox spreads quickly through schools and other places of close contact. Once someone has been infected with the disease, they usually develop protective immunity for life. It is fairly rare to get the chickenpox multiple times, but it is possible for people with irregular immune systems. As the disease is more severe if contracted by an adult, parents have been known to ensure their children become infected before adulthood.
The disease is rarely fatal: if fatality occurs, the actual death is usually from varicella pneumonia, and occurs more frequently in pregnant women. In the US, 55 percent of chickenpox deaths were in the over-20 age group. Doctors advise pregnant women not known to be immune and who come into contact with chickenpox should contact their doctor immediately, as the virus can cause serious problems for the fetus. In the UK Varicella antibodies are measured as part of the routine of antenatal care, and by 2005 all NHS healthcare personnel had determined their immunity and been immunised if they were non-immune.
Later in life, viruses remaining in the nerves can develop into the painful disease shingles, particularly in people with compromised immune systems, such as the elderly, and perhaps even those suffering sunburn. Some of these will develop zoster-associated pain or post-herpetic neuralgia, described usually as "horrible" or "excruciating". A chickenpox vaccine has been available since 1995, and is now required in some countries for children to be admitted into elementary school. In addition, effective medications (e.g., aciclovir) are available to treat chickenpox in healthy and immunocompromised persons. Symptomatic treatment—calamine lotion to ease itching and paracetamol to reduce fever—is widely used. Aspirin is contraindicated in children with chickenpox, as it can lead to Reye's syndrome.
HistoryOne history of medicine book claims Giovanni Filippo (1510–1580) of Palermo gave the first description of varicella (chickenpox). Subsequently in the 1600s, an English physician named Richard Morton described what he thought was a mild form of smallpox as "chicken pox." Later, in 1767, a physician named William Heberden, also from England, was the first physician to clearly demonstrate that chickenpox was different from smallpox. However, it is believed the name chickenpox was commonly used in earlier centuries before doctors identified the disease.
There are many explanations offered for the origin of the name chickenpox:
* the specks that appear looked as though the skin was picked by chickens,
* the disease was named after chick peas, from a supposed similarity in size of the seed to the lesions
* Samuel Johnson suggested that the disease was "no very great danger," thus a "chicken" version of the pox
* the term reflects a corruption of the Old English word, "giccin", which meant "itching"
As "pox" also means curse, in medieval times some believed it was a plague brought on to curse children by the use of black magic.
During the medieval era, oatmeal was discovered to soothe the sores, and oatmeal baths are today still commonly given to relieve itching.
InfectionChickenpox is highly infectious and spreads from person to person by direct contact or through the air from an infected person’s coughing or sneezing. Touching the fluid from a chicken pox blister can also spread the disease. A persons with chickenpox is contagious 1-2 days before the rash appears and until all blisters have formed scabs. This may take between 5-10 days[1]. It takes from 10-21 days after contact with an infected person for someone to develop chickenpox.
The chicken pox lesions (blisters) start as a 2-4 mm red papule which develops an irregular outline (rose petal). A thin-walled, clear vesicle (dew drop) develops on top of the area of redness. This "dew drop on a rose petal" lesion is very characteristic for chicken pox. After about 8-12 hours the fluid in the vesicle gets cloudy and the vesicle breaks leaving a crust. The fluid is highly contagious, but once the lesion crusts over, it is not considered contagious. The crust usually falls off after 7 days sometimes leaving a craterlike scar. Although one lesion goes through this complete cycle in about 7 days, another hallmark of chicken pox is the fact that new lesions crop up every day for several days. Therefore, it may take about a week until new lesions stop appearing and existing lesions crust over. Children are not sent back to school until all lesions have crusted over.
The contagious period for chickenpox begins about 2 days before the rash appears and lasts until all the blisters are crusted over. A child with chickenpox should be kept out of school until all of the blisters have dried, which is usually about 1 week, but you don't have to wait until all the scabs fall off to let your child get back to a normal schedule.
It is a debated fact as to whether a person, once infected with Chicken Pox can contract the disease again. Although numerous sources claim it is not possible, there have been reported cases of repeat infections.
VaccinationRoutine vaccination against varicella zoster virus is performed mainly in the United States, and the incidence of chickenpox has been dramatically reduced there (from 4 million cases per year in the pre-vaccine era to approximately 400,000 cases per year as of 2005). In Europe most countries do not currently vaccinate against varicella, though the vaccine is gaining wider acceptance. Australia, Canada, and other countries have now adopted recommendations for routine immunization of children and susceptible adults against chickenpox. Other countries, such as Germany and The United Kingdom have targeted recommendations for the vaccine, e.g. for susceptible health care workers at risk of varicella exposure.
Chickenpox is most often a mild disease -- especially for children. Prior to the introduction of vaccine, there were around 4,000,000 cases per year in the US, mostly children, yet typically 100 or fewer people died. Though mostly children caught it, the majority of deaths (by as much as 80%) were among adults. Additionally, chickenpox involved the hospitalization of about 10,000 people each year. During 2003 and the first half of 2004, the CDC reported eight deaths from varicella, six of whom were children or adolescents. These deaths and hospitalizations have substantially declined in the US due to vaccination, though the rate of shingles infection has increased for the same reason. The vaccine has more recently been determined to be effective at preventing shingles (zoster) in persons 60 years of age and older, if administered regularly.
The long-term duration of protection from varicella vaccine is unknown, but there are now persons vaccinated more than thirty years ago with no evidence of waning immunity, while others have become vulnerable in as few as 6 years. Assessments of duration of immunity are complicated in an environment where natural disease is still common, which typically leads to an overestimation of effectiveness, and we are only now entering an era in the US where the long-term efficacy of varicella vaccine can be accurately gauged (Goldman, 2005).
CHAGAS DISEASE
Chagas disease (also called American trypanosomiasis) is a human tropical parasitic disease which occurs in the Americas, particularly in South America. Its pathogenic agent is a flagellate protozoan named Trypanosoma cruzi, which is transmitted to humans and other mammals mostly by hematophagous insects of the subfamily Triatominae (Family Reduviidae). Those insects are known by numerous common names varying by country, including assassin bug, benchuca, vinchuca, kissing bug, chipo, barbeiro, et cetera. The most common insect species belong to the genera Triatoma, Rhodnius, and Panstrongylus. Other forms of transmission are possible, though, such as ingestion of food contaminated with parasites, blood transfusion and fetal transmission.
Trypanosoma cruzi is a member of the same genus as the infectious agent of African sleeping sickness, but its clinical manifestations, geographical distribution, life cycle and insect vectors are quite different.
HistoryThe disease was named after the Brazilian physician and infectologist Carlos Chagas, who first described it in 1909, but the disease was not seen as a major public health problem in humans until the 1960s. He discovered that the intestines of Triatomidae harbored a flagellate protozoan, a new species of the Trypanosoma genus, and was able to prove experimentally that it could be transmitted to marmoset monkeys which were bitten by the infected bug.
Chagas named the pathogenic parasite that causes the disease Schizotrypanum cruzi (later renamed to Trypanosoma cruzi), after Oswaldo Cruz, the noted Brazilian physician and epidemiologist who fought successfully epidemics of yellow fever, smallpox, and bubonic plague in Rio de Janeiro and other cities in the beginning of the 20th century. Chagas’ work is unique in the history of medicine, because he was the only researcher so far to describe completely a new infectious disease: its pathogen, vector, host, clinical manifestations, and epidemiology. Nevertheless, he at least believed falsely until 1925, that the main infection route is by the sting of the insect and not by the feces, as it was proposed by his colleague Emile Brumpt 1915 and assured by Dias 1932, Cardoso 1938 and Brumpt himself 1939.
On another historical point of view, it has been hypothesized that Charles Darwin might have suffered from this disease as a result of a bite of the so-called Great Black Bug of the Pampas (vinchuca) (see Illness of Charles Darwin). The episode was reported by Darwin in his diaries of the Voyage of the Beagle as occurring in March 1835 to the east of the Andes near Mendoza. Darwin was young and in general good health though six months previously he had been ill for a month near Valparaiso, but in 1837, almost a year after he returned to England, he began to suffer intermittently from a strange group of symptoms, becoming very incapacitated for much of the rest of his life. Attempts to test Darwin's remains at the Westminster Abbey by using modern PCR techniques were met with a refusal by the Abbey's curator.
Epidemiology and geographical distributionChagas disease currently affects 16-18 million people, killing around 20,000 people annually and with some 100 million at risk of acquiring the disease. Chronic Chagas disease remains a major health problem in many Latin American countries, despite the effectiveness of hygienic and preventive measures, such as eliminating the transmitting insects, which have reduced to zero new infections in at least two countries of the region. With increased population movements, however, the possibility of transmission by blood transfusion has become more substantial in the United States. Also, T. cruzi has already been found infecting wild opossums and raccoons as far as North Carolina.
The disease is distributed in the Americas, ranging from the southern United States to southern Argentina, mostly in poor, rural areas of Central and South America.
The disease is almost exclusively found in rural areas, where the Triatominae can breed and feed on the natural reservoirs (the most common ones being opossums and armadillos) of T.cruzi. Depending on the special local interactions of the vectors and their hosts, other infected humans, domestic animals like cats, dogs, guinea pigs and wild animals like rodents, monkeys, ground squirrels (Spermophilus beecheyi) and many other could also serve as important parasite reservoirs. Though Triatominae bugs feed on birds, these seem to be immune against infection and therefore are not considered to be a T. cruzi reservoir, but they remain suspicious to be a constant feeding resource for the vectors in the surroundings of human stay.
The popular name of the vector insect in Brazil, barbeiro ("the barber"), so called because it sucks the blood at night by biting the face of its victims, reveals some of its habits. The insects, who develop a predominantly domiciliary and anthropophilic behaviour once they have infested a house, usually hide during the day in crevices and gaps in the walls and roofs of poorly constructed homes. More rarely, better constructed houses may harbor the insect vector, due to the use of rough materials for making roofs, such as bamboo and thatch. A mosquito net, wrapped under the mattress, will provide protection in these situations, when the adult insect might sail down from above, but one of the five nymphal stages (instars) could crawl up from the floor.
Even when the colonies of the insects are eradicated in the house and around (domestic animal shelters), they again can arrive (also by flying short distances) from nearby nature (possibly a palm tree), where animals and the insect which are part of the ancient, natural silvatic infection cycle use to live. This especially can happen in zones with mixed open savannah, clumps of trees, etc., interspersed by human habitation.
Dense vegetation, like in tropical rain forests, and urban habitats, are not ideal for the establishment of the human transmission cycle. However, in regions where the sylvatic habitat and its fauna are thinned out by economical exploitation and human habitation, such as in newly deforested areas of the Amazon region, this may occur, when the insects are searching for a new prey.
Clinical manifestationsThe human disease occurs in two stages: the acute stage shortly after the infection, and the chronic stage that may develop over 10 years.
In the acute phase, a local skin nodule called a chagoma can appear at the site of inoculation. When the inoculation site is the conjunctival mucous membranes, the patient may develop unilateral periorbital edema, conjunctivitis, and preauricular lymphadenitis. This constellation of findings is referred to as Romaña's sign. The acute phase is usually asymptomatic, but can present with manifestations that include fever, anorexia, lymphadenopathy, mild hepatosplenomegaly, and myocarditis. Some acute cases (10 to 20%) resolve over a period of 2 to 3 months into an asymptomatic chronic stage, only to reappear after several years.
The symptomatic chronic stage may not occur for years or even decades after initial infection. The disease affects the nervous system, digestive system and heart. Chronic infections result in various neurological disorders, including dementia, damage to the heart muscle (cardiomyopathy, the most serious manifestation), and sometimes dilation of the digestive tract (megacolon and megaesophagus), as well as weight loss. Swallowing difficulties may be the first symptom of digestive disturbances and may lead to malnutrition. After several years of an asymptomatic period, 27% of those infected develop cardiac damage, 6% develop digestive damage, and 3% present peripheral nervous involvement. Left untreated, Chagas disease can be fatal, in most cases due to the cardiomyopathy component.
Laboratory diagnosisDemonstration of the causal agent is the diagnostic procedure in acute Chagas disease. It almost always yields positive results, and can be achieved by:
* Microscopic examination: a) of fresh anticoagulated blood, or its buffy coat, for motile parasites; and b) of thin and thick blood smears stained with Giemsa, for visualization of parasites; it can be confused with the 50% longer Trypanosoma rangeli, which has not shown any pathogenity in humans yet.
* Isolation of the agent by: a) inoculation into mice; b) culture in specialized media (e.g. NNN, LIT); and c) xenodiagnosis, where uninfected Reduviidae bugs are fed on the patient's blood, and their gut contents examined for parasites 4 weeks later.
* Various Immunodiagnostic tests; (also trying to distinguish strains (zymodemes) of T.cruzi with divergent pathogenities).
o Complement fixation
o indirect hemagglutination
o IFA, Indirect fluorescent assay
o RIA, Radio-immunoassay
o ELISA, Enzyme-Linked Immunosorbent Assay
o PCR, Polymerase chain reaction, most promising
TreatmentMedication for Chagas disease is usually only effective when given during the acute stage of infection. The drugs of choice are azole or nitroderivatives such as benznidazole or nifurtimox (under an Investigational New Drug protocol from the CDC Drug Service), but resistance to these drugs has already been reported. Furthermore, these agents are very toxic and have many adverse effects, and cannot be taken without medical supervision. A 10-year study of chronic administration of drugs in Brazil has revealed that these drugs are not totally effective, too, in removing parasitemia. Thus, the decision about whether to use antiparasitic therapy should be individualized in consultation with an expert.
In the chronic stage, treatment involves managing the clinical manifestations of the disease, e.g., drugs and heart pacemaker for chronic heart failure and heart arryhthmias; surgery for megaintestine, etc., but the disease per se is not curable in this phase. Chronic heart disease caused by Chagas is now a common reason for heart transplantation surgery. Until recently, however, Chagas disease was considered a contraindication for the procedure, since the heart damage could recur as the parasite was expected to seize the opportunity provided by the immunosuppression that follows surgery. The research that changed the indication of the transplant procedure for Chagas disease patients was conducted by Dr. Adib Jatene's group at the Heart Institute of the University of São Paulo, in São Paulo, Brazil. The research noted that survival rates in Chagas patients can be significantly improved by using lower dosages of the immunosuppressant drug cyclosporine. Recently, direct stem cell therapy of the heart muscle using bone marrow cell transplantation has been shown to dramatically reduce risks of heart failure in Chagas patients. Patients have also been shown to benefit from the strict prevention of reinfection, though the reason for this is not yet clearly understood.
Some examples for the struggle for advances:
* Use of oxidosqualene cyclase inhibitors and cysteine protease inhibitors has been found to cure experimental infections in animals.
* Dermaseptins from frog species Phyllomedusa oreades and P. distincta. Anti-Trypanosoma cruzi activity without cytotoxicity to mammalian cells.
* The sesquiterpene lactone dehydroleucodine (DhL) affects the growth of cultured epimastigotes of Trypanosoma cruzi
* The genome of the disease has been sequenced. Proteins that are produced by the disease but not by humans have been identified as possible drug targets to defeat the disease.
PreventionA reasonably effective vaccine was developed in Ribeirão Preto in the 1970s, using cellular and subcellular fractions of the parasite, but it was found economically unfeasible. More recently, the potential of DNA vaccines for immunotherapy of acute and chronic Chagas disease is being tested by several research groups.
Prevention is centered on fighting the vector (Triatoma) by using sprays and paints containing insecticides (synthetic pyrethroids), and improving housing and sanitary conditions in the rural area. For urban dwellers, spending vacations and camping out in the wilderness or sleeping at hostels or mud houses in endemic areas can be dangerous, a mosquito net is recommended. If the traveller intends to travel to the area of prevalence, he/she should get information on endemic rural areas for Chagas disease in traveller advisories, such as the CDC.
In most countries where Chagas disease is endemic, testing for blood donors is already mandatory, since this can be an important route of transmission. In the past, blood donors where mixed with 0,25 g/L of gentian violet successfully to kill parasites.
With all these measures, some landmarks were achieved in the fight against Chagas disease in Latin America: a reduction by 72% of the incidence of human infection in children and young adults in the countries of the Initiative of the Southern Cone, and at least two countries (Uruguay, in 1997, and Chile, in 1999), were certified free of vectorial and transfusional transmission. In Brazil, with the largest population at risk, 10 out of the 12 endemic states were also certified free.
Some stepstones of vector control:
* A yeast trap has been tested for monitoring infestations of certain species of the bugs:"Performance of yeast-baited traps with Triatoma sordida, Triatoma brasiliensis, Triatoma pseudomaculata, and Panstrongylus megistus in laboratory assays."
* Promising results were gained with the treatment of vector habitats with the fungus Beauveria bassiana, (which is also in discussion for malaria- prevention):"Activity of oil-formulated Beauveria bassiana against Triatoma sordida in peridomestic areas in Central Brazil."
* Targeting the symbionts of Triatominae
CROUPCroup (also called laryngotracheobronchitis) is a disease which afflicts infants and young children, typically aged between 3 months and 5 years.
SymptomsIt is characterized by a harsh 'barking' cough, stridor and fever.
The 'barking' cough of croup is diagnostic.
In diagnosing croup, it is important for the physician to consider and exclude other causes of shortness of breath.
CausesIt is most often caused by parainfluenza virus, but other viral and bacterial infections can also cause it. It is the body's reaction to the infection that causes the respiratory distress, not the infection itself. It usually occurs in young children as their airways are smaller and differently shaped than adults, making them more susceptible. There is some element of genetic predisposition as children in some families are more susceptible than others.
TreatmentTreatment of croup depends on the severity encountered.
* One of the simplest ways to treat or help with croup is to take hot showers that steam (the steam moisturizes the airway) or just use a humidifier, which has a similar effect. These simple methods usually help a lot. However, they may not be enough to completely get rid of the croup in moderate to severe cases.
* Mild croup with no stridor and just the cough may just be watched or a small dose of inhaled or oral steroids may be given.
* Moderate to severe croup may require airway intervention and oxygen supplementation in addition to steroids, depending on the amount of respiratory distress.
* Adrenaline may also be given in cases of severe croup, either via nebulizer or injected intramuscularly or intravenously.
CYTOMEGALOVIRUSCytomegalovirus (CMV), is a genus of Herpes viruses; in humans the species is known as Human herpesvirus 5 (HHV-5). It belongs to the Betaherpesvirinae subfamily of Herpesviridae. The name means "cell very big virus".
CMV especially attacks salivary glands and may also be devastating or even fatal to fetuses. CMV infection can also be life threatening for patients who are immunocompromised (e.g. patients with HIV or organ transplant recipients). CMV viruses are found in many mammal species, but generally are specific only to that species.
Species
* Cercopithecine herpesvirus 5 (CeHV-5) - African green monkey cytomegalovirus
* Cercopithecine herpesvirus 8 (CeHV-8) - Rhesus monkey cytomegalovirus
* Human herpesvirus 5 (HHV-5) - Human cytomegalovirus
* Pongine herpesvirus 4 (PoHV-4)
Tentative species:
* Aotine herpesvirus 1 (AoHV-1) - Herpesvirus aotus 1
* Aotine herpesvirus 3 (AoHV-3) - Herpesvirus aotus 3
General informationCytomegalovirus, or CMV, is found universally throughout all geographic locations and socioeconomic groups, and infects between 50% and 85% of adults in the United States by 40 years of age. CMV is also the virus most frequently transmitted to a developing child before birth. CMV infection is more widespread in developing countries and in areas of lower socioeconomic conditions. For most healthy persons who acquire CMV after birth there are few symptoms and no long-term health consequences. Some persons with symptoms experience infectious mononucleosis, with prolonged fever, and a mild hepatitis. A very sore throat is also common. Once a person becomes infected, the virus latently persists in the body for the person's life. Recurrent disease rarely occurs unless the person's immune system is suppressed due to therapeutic drugs or disease. Therefore, for the vast majority of people, CMV infection is not a serious problem.
However, CMV infection is important to certain high-risk groups. Major areas of concern are (1) the risk of infection to the unborn baby during pregnancy, (2) the risk of infection to people who work with children, and (3) the risk of infection to the immunocompromised person, such as organ transplant recipients and persons infected with human immunodeficiency virus (HIV).
The virus acts by blocking cell apoptosis via the mitochondria and causing massive cell enlargement, which is the source of the virus' name.
Characteristics of the virusCMV is a member of the herpesvirus group, which includes herpes simplex virus types 1 and 2, varicella-zoster virus (which causes chickenpox and shingles), and Epstein-Barr virus (which, together with CMV, is the main cause for infectious mononucleosis). These viruses share a characteristic ability to remain latent within the body over a long period.
Initial CMV infection, which may have few symptoms, is always followed by a prolonged, inapparent infection during which the virus resides in cells without causing detectable damage or clinical illness. Severe impairment of the body's immune system by medication or disease (see below) may reactivate the virus from the latent or dormant state.
Infectious CMV may be shed in the bodily fluids of any previously infected person, and thus may be found in urine, saliva, blood, tears, semen, and breast milk. The shedding of virus may take place intermittently, without any detectable signs, and without causing symptoms.
As a result of efforts to create an attenuated-virus vaccine, there currently exist two general classes of CMV. Clinical isolates comprise those viruses obtained from patients and represent the wild-type viral genome, while laboratory strains have been cultured extensively in the lab setting and typically contain numerous accumulated mutations. Most notably, the laboratory strain AD169 appears to lack a 15kb region of the 200kb genome that is present in clinical isolates. This region contains 19 open reading frames whose functions have yet to be elucidated. AD169 is also unique in that it is unable to enter latency and nearly always assumes lytic growth upon infection.
Transmission and preventionTransmission of CMV occurs from person to person. Infection requires close, intimate contact with a person excreting the virus in their saliva, urine, or other bodily fluids. CMV can be sexually transmitted and can also be transmitted via breast milk, transplanted organs, and rarely from blood transfusions.
Although the virus is not highly contagious, it has been shown to spread in households and among young children in day care centers. Transmission of the virus is often preventable because it is most often transmitted through infected bodily fluids that come in contact with hands and then are absorbed through the nose or mouth of a susceptible person. Therefore, care should be taken when handling children and items like diapers. Simple hand washing with soap and water is effective in removing the virus from the hands.
CMV infection without symptoms is common in infants and young children; as a result, it is common to not exclude from school or an institution a child known to be infected. Similarly, hospitalized patients are not typically separated or isolated.
Specific situationsPregnancyThe incidence of primary (or first) CMV infection in pregnant women in the United States varies from 1% to 3%. Healthy pregnant women are not at special risk for disease from CMV infection. When infected with CMV, most women have no symptoms and very few have a disease resembling mononucleosis. It is their developing unborn babies that may be at risk for congenital CMV disease. CMV remains the most important cause of congenital (meaning from birth) viral infection in the United States. For infants who are infected by their mothers before birth, two potential problems exist:
* Generalized infection may occur in the infant, and symptoms may range from moderate enlargement of the liver and spleen (Hepatosplenomegaly) (with jaundice) to fatal illness. With supportive treatment most infants with CMV disease usually survive. However, from 80% to 90% will have complications within the first few years of life that may include hearing loss, vision impairment, and varying degrees of mental retardation.
* Another 5% to 10% of infants who are infected but without symptoms at birth will subsequently have varying degrees of hearing and mental or coordination problems.
However, these risks appear to be almost exclusively associated with women who previously have not been infected with CMV and who are having their first infection with the virus during pregnancy. Even in this case, two-thirds of the infants will not become infected, and only 10% to 15% of the remaining third will have symptoms at the time of birth. There appears to be little risk of CMV-related complications for women who have been infected at least 6 months prior to conception. For this group, which makes up 50% to 80% of the women of child-bearing age, the rate of newborn CMV infection is 1%, and these infants appear to have no significant illness or abnormalities.
The virus can also be transmitted to the infant at delivery from contact with genital secretions or later in infancy through breast milk. However, these infections usually result in little or no clinical illness in the infant.
To summarize, during a pregnancy when a woman who has never had CMV infection becomes infected with CMV, there is a potential risk that after birth the infant may have CMV-related complications, the most common of which are associated with hearing loss, visual impairment, or diminished mental and motor capabilities. On the other hand, infants and children who acquire CMV after birth have few, if any, symptoms or complications.
Recommendations for pregnant women with regard to CMV infection:
* Throughout the pregnancy, practice good personal hygiene, especially handwashing with soap and water, after contact with diapers or oral secretions (particularly with a child who is in day care).
* Women who develop a mononucleosis-like illness during pregnancy should be evaluated for CMV infection and counseled about the possible risks to the unborn child.
* Laboratory testing for antibody to CMV can be performed to determine if a women has already had CMV infection.
* Recovery of CMV from the cervix or urine of women at or before the time of delivery does not warrant a cesarean section.
* The demonstrated benefits of breast-feeding outweigh the minimal risk of acquiring CMV from the breast-breeding mother.
* There is no need to either screen for CMV or exclude CMV-excreting children from schools or institutions because the virus is frequently found in many healthy children and adults.
ChildcareMost healthy people working with infants and children face no special risk from CMV infection. However, for women of child-bearing age who previously have not been infected with CMV, there is a potential risk to the developing unborn child (the risk is described above in the Pregnancy section). Contact with children who are in day care, where CMV infection is commonly transmitted among young children (particularly toddlers), may be a source of exposure to CMV. Since CMV is transmitted through contact with infected body fluids, including urine and saliva, child care providers (meaning day care workers, special education teachers, therapists, as well as mothers) should be educated about the risks of CMV infection and the precautions they can take. Day care workers appear to be at a greater risk than hospital and other health care providers, and this may be due in part to the increased emphasis on personal hygiene in the health care setting.
Recommendations for individuals providing care for infants and children:
* Female employees should be educated concerning CMV, its transmission, and hygienic practices, such as handwashing, which minimize the risk of infection.
* Susceptible nonpregnant women working with infants and children should not routinely be transferred to other work situations.
* Pregnant women working with infants and children should be informed of the risk of acquiring CMV infection and the possible effects on the unborn child.
* Routine laboratory testing for CMV antibody in female workers is not recommended, but can be performed to determine their immune status
Immunocompromised patientsPrimary (or the initial) CMV infection in the immunocompromised patient can cause serious disease. However, the more common problem is the reactivation of the latent virus.
In patients with a depressed immune system, CMV-related disease may be much more aggressive. CMV hepatitis may cause fulminant liver failure. Specific disease entities recognised in those people are cytomegalovirus retinitis (inflammation of the retina, characterised by a "pizza pie appearance" on ophthalmoscopy) and cytomegalovirus colitis (inflammation of the large bowel).
Infection with CMV is a major cause of disease and death in immunocompromised patients, including organ transplant recipients, patients undergoing hemodialysis, patients with cancer, patients receiving immunosuppressive drugs, and HIV-infected patients. Because of this risk, exposing immunosuppressed patients to outside sources of CMV should be minimized. Whenever possible, patients without CMV infection should be given organs and/or blood products that are free of the virus.
Patients without CMV infection who are given organ transplants from CMV-infected donors should be given prophlyactic treatment with valganciclovir (ideally) or ganciclovir and require regular serological monitoring to detect a rising CMV titre, which should be treated early to prevent a potentially life-threatening infection becoming established.
Diagnosis of infectionMost infections with CMV are not diagnosed because the virus usually produces few, if any, symptoms and tends to reactivate intermittently without symptoms. However, persons who have been infected with CMV develop antibodies to the virus, and these antibodies persist in the body for the lifetime of that individual. A number of laboratory tests that detect these antibodies to CMV have been developed to determine if infection has occurred and are widely available from commercial laboratories. In addition, the virus can be cultured from specimens obtained from urine, throat swabs, bronchial lavages and tissue samples to detect active infection. Both qualitative and quantitative PCR testing for CMV are available as well, allowing physicians to monitor the viral load of CMV-infected patients.
CMV should be suspected if a patient:
* Has symptoms of infectious mononucleosis but has negative test results for mononucleosis and Epstein Barr virus, or,
* Shows signs of hepatitis, but has negative test results for hepatitis A, B, and C.
For best diagnostic results, laboratory tests for CMV antibody should be performed by using paired serum samples. One blood sample should be taken upon suspicion of CMV, and another one taken within 2 weeks. A virus culture can be performed at any time the patient is symptomatic.
Laboratory testing for antibody to CMV can be performed to determine if a woman has already had CMV infection. However, routine laboratory testing of all pregnant women is costly and the need for testing should therefore be evaluated on a case-by-case basis.
Serologic testingThe enzyme-linked immunosorbent assay (or ELISA) is the most commonly available serologic test for measuring antibody to CMV. The result can be used to determine if acute infection, prior infection, or passively acquired maternal antibody in an infant is present. Other tests include various fluorescence assays, indirect hemagglutination, polymerase chain reaction (PCR) and latex agglutination.
An ELISA technique for CMV-specific IgM is available, but may give false-positive results unless steps are taken to remove rheumatoid factor or most of the IgG antibody before the serum sample is tested. Because CMV-specific IgM may be produced in low levels in reactivated CMV infection, its presence is not always indicative of primary infection. Only virus recovered from a target organ, such as the lung, provides unequivocal evidence that the current illness is caused by acquired CMV infection. If serologic tests detect a positive or high titer of IgG, this result should not automatically be interpreted to mean that active CMV infection is present. However, if antibody tests of paired serum samples show a fourfold rise in IgG antibody and a significant level of IgM antibody, meaning equal to at least 30% of the IgG value, or virus is cultured from a urine or throat specimen, the findings indicate that an active CMV infection is present.
Relevance to blood donorsAlthough the risks discussed above are generally low, CMV assays are part of the standard screening for non-directed blood donation (donations not specified for a particular patient) in the U.S. CMV-negative donations are then earmarked for transfusion to infants or immunocompromised patients. Some blood donation centers may maintain lists of donors whose blood is CMV negative due to special demands.
TreatmentNo treatment is generally necessary for CMV infection in the healthy individual since the majority of infections resolve on their own. Antiviral drug therapy is now being evaluated in infants.
Ganciclovir treatment is used for patients with depressed immunity who have either sight-related or life-threatening illnesses. Valganciclovir (marketed as Valcyte) is an antiviral drug that is also effective and is given orally. Foscarnet can be given in patients with CMV resistant to ganciclovir, though foscarnet is not as well tolerated as ganciclovir.
Vaccines are still in the research and development stage.
DUCHENNE MUSCULAR DYSTROPHYDuchenne muscular dystrophy (DMD) (also known as muscular dystrophy - Duchenne type) is an inherited disorder characterized by rapidly progressive muscle weakness which starts in the legs and pelvis and later affects the whole body. Duchenne muscular dystrophy (DMD) is the most common form of muscular dystrophy. It usually affects only boys, but in rare cases it can also affect girls. It is an X-linked recessive inherited disease. A milder form of this disease is known as Becker Muscular dystrophy (BMD). In Becker muscular dystrophy, most of the symptoms are similar to Duchenne, but the onset is later and the course is milder.
DMD is named after the French neurologist Guillaume Benjamin Amand Duchenne (1806-1875), who first described the disease in the 1860s. One third of the cases are known to be caused by development of spontaneous mutations in the dystrophin gene, while the remainder are inherited. Boys with DMD develop weak muscles because the muscle fibers that were present at birth are destroyed. It is due to mutations in the dystrophin gene, which encodes a cell membrane protein in myocytes (muscle cells).
GeneticsDuchenne dystrophy is a type of dystrophinopathy which includes a spectrum of muscle disease caused by mutations in the DMD gene, which encodes the protein dystrophin. Becker's muscular dystrophy is a milder type of dystrophinopathy. Although it is caused by a defective gene, it often occurs in people from families without a known family history of the condition.
Duchenne muscular dystrophy is inherited in an X-linked recessive pattern. This means that women are almost never affected; women normally have two X chromosomes, one of which contains a normal, dominant copy of the gene that will make enough of the protein for them to avoid symptoms. Women who carry the defective gene can pass an abnormal X on to their sons, however. Since boys have an X from their mother and a Y from father, there is no second X to make up for the defective gene from the carrier mother. The sons of carrier females each have a 50% chance of having the disease, and the daughters each have a 50% chance of being carriers. Daughters of men with Duchenne will always be carriers, since they will inherit an affected X chromosome from their father (note that the diagram only shows the results from an unnaffected father).
Prenatal testing, such as amniocentesis, for pregnancies at risk is possible if the DMD disease-causing mutation has been identified in a family member or if informative linked markers have been identified.
In 30% of the cases, the disease is a result of a spontaneous mutation.
In some female cases, DMD is caused by skewed x inactivation. In these cases, two copies of the x chromosome exist, but for reasons currently unknown, the flawed x chromosome manifests instead of the unflawed copy. In these cases, a mosaic form of DMD is seen, in which some muscle cells are completely normal while others exhibit classic DMD findings. The effects of a mosaic form of DMD on long-term outlook is not known.
Symptoms * Muscle weakness
* Rapidly progressive
* Frequent falls
* Difficulty with motor skills (running, hopping, jumping)
* Progressive difficulty walking
* Ability to will be lost by age 11
* Fatigue
* Intellectual impairment (in approx. 30% of Duchenne's patients)
* Skeletal deformities
* Chest and back (scoliosis)
* Muscle deformities
* Contractures of heels, legs
* Pseudohypertrophy of tongue and calf muscles
* Mild mental retardation in some cases
Symptoms usually appear before age 6 and may appear as early as infancy. There is progressive muscle weakness of the legs and pelvis, which is associated with a loss of muscle mass (wasting). Muscle weakness also occurs in the arms, neck, and other areas, but not as severely or as early as in the lower half of the body. Calf muscles initially enlarge -- the enlarged muscle tissue is eventually replaced by fat and connective tissue (pseudohypertrophy). Muscle contractures occur in the legs, rendering the muscles unusable because the muscle fibers shorten and fibrosis occurs in connective tissue.
TreatmentThere is no known cure for Duchenne muscular dystrophy. Treatment is aimed at control of symptoms to maximize the quality of life. Physical activity is encouraged. Inactivity (such as bed rest) can worsen the muscle disease. Physical and occupational therapy may be helpful to maintain muscle strength and function. Orthopaedic appliances (such as braces and wheelchairs) may improve mobility and the ability for self-care.
MEASLESMeasles, also known as rubeola, is a disease caused by a virus of the genus Morbillivirus.
Reports of measles go back to at least 700, however, the first scientific description of the disease and its distinction from smallpox is attributed to the Persian physician Ibn Razi (Rhazes) 860-932 who published a book entitled "Smallpox and Measles" (in Arabic: Kitab fi al-jadari wa-al-hasbah). In 1954, the virus causing the disease was isolated, and licensed vaccines to prevent the disease became available in 1963.
Measles is spread through respiration (contact with fluids from an infected person's nose and mouth, either directly or through aerosol transmission), and is highly contagious - 90% of people without immunity sharing a house with an infected person will catch it. Airborne precautions should be taken for all suspected cases of measles.
The incubation period usually lasts for 10-12 days (during which there are no symptoms).
Infected people remain contagious from the appearance of the first symptoms until 3-5 days after the rash appears.
SymptomsThe classical symptoms of measles include a fever for at least three days duration, and the three C's - cough, coryza (runny nose) and conjunctivitis (red eyes). The fever may reach up to 40 degrees Celsius (105 Fahrenheit). Koplik's spots seen inside the mouth are pathognomic (diagnostic) for measles but are not often seen, even in real cases of measles, because they are transient and may disappear within a day of arising.
The rash in measles is classically described as a generalised, maculopapular, erythematous rash that begins several days after the fever starts. It starts on the head before spreading to cover most of the body. The measles rash also classically "stains" by changing colour to dark brown from red before disappearing later. The rash can be itchy.
DiagnosisA detailed history should be taken including course of the disease so far, vaccination history, contact history, and travel history.
Clinical diagnosis of measles requires a history of fever of at least three days together with at least one of the three Cs above. Observation of Koplik's spots is also diagnostic of measles.
Alternatively, laboratory diagnosis of measles can be done with confirmation of positive measles IgM antibodies or isolation of measles virus RNA from respiratory specimens.
Positive contact with other patients known to have measles adds strong epidemiological evidence to the diagnosis.
TreatmentThere is no specific treatment for uncomplicated measles. Patients with uncomplicated measles will recover with rest and supportive treatment.
ComplicationsComplications with measles are relatively common, ranging from relatively common and less serious diarrhea, to pneumonia and encephalitis (subacute sclerosing panencephalitis). Complications are usually more severe amongst adults who catch the virus.
The fatality rate from measles for otherwise healthy people in developed countries is low: approximately 1 death per thousand cases. In underdeveloped nations with high rates of malnutrition and poor healthcare, fatality rates of 10 percent are common. In immunocompromised patients, the fatality rate is approximately 30 percent.
Public healthIn developed countries, most children are immunised against measles at the age of 18 months, generally as part of a three-part MMR vaccine (measles, mumps, and rubella). The vaccination is generally not given earlier than this because children younger than 18 months usually retain anti-measles immunoglobulins (antibodies) transmitted from the mother during pregnancy. A "booster" vaccine is then given between the ages of four and five. Vaccination rates have been high enough to make measles relatively uncommon. Even a single case in a college dorm or similar setting is often met with a local vaccination program, in case any of the people exposed are not already immune. In developing countries, measles remains common.
The recent vaccine controversy in the UK regarding a potential link between the combined MMR vacine (vaccinating children from mumps, measles and rubella) and autism has prompted a resurgence in popularity of the "measles party", where parents deliberately infect the child with measles in order to build up the child's immunity without requiring an injection. This practice poses many health risks to the child, and has been discouraged by the UK's National Health Service.
Measles is a significant infectious disease because, while the rate of complications is not high, the disease itself is so infectious that the sheer number of people who would suffer complications in an outbreak amongst non-immune people would quickly overwhelm available hospital resources. If vaccination rates fall, the number of non-immune persons in the community rises and the risk of an outbreak of measles consequently rises.
According to the World Health Organization (WHO), measles is a leading cause of vaccine preventable childhood mortality - there were 30 million cases and 875,000 deaths caused by measles every year.The WHO and the United Nations Children's Fund (UNICEF) reports that the global immunization drive has cut measles deaths by nearly half between 1999 and 2004 (from 871,000 in 1999 to an estimated 454,000 in 2004), "thanks to major national immunization activities and better access to routine childhood immunization".
MUMPSMumps or epidemic parotitis is a viral disease of humans. Prior to the development of vaccination, it was a common childhood disease worldwide, and is still a significant threat to health in the third world.
Symptoms of mumps tend to be mild, such as painful swelling of the salivary glands and testicles, rash and fever. In teenagers and adults, the symptoms can be more severe and complications (such as infertility or subfertility (see PMID 8692089, PMID 2368216, PMID 2100952) are relatively common, although still rare in absolute terms. The disease is generally self-limiting, and there is no specific treatment apart from controlling the symptoms with painkillers.
Causes and risksThe mumps are caused by a paramyxovirus, and is spread from person to person by saliva droplets or direct contact with articles that have been contaminated with infected saliva. The parotid glands (the salivary glands between the ear and the jaw) are usually involved. Unvaccinated children between the ages of 2 and 12 are most commonly infected, but the infection can occur in other age groups. Orchitis (swelling of the testes) occurs in 10-20% of infected males, but sterility only rarely ensues; a viral meningitis occurs in about 5% of those infected. In older people, other organs may become involved including the central nervous system, the pancreas, the prostate, the breasts, and other organs.
The incubation period is usually 12 to 24 days. Mumps is generally a mild illness in children in developed countries. After adolescence, mumps tends to affect the ovary, causing oophoritis, and the testis, causing orchitis. The mature testis is particularly susceptible to damage from mumps which can lead to infertility. Adults infected with mumps are more likely to develop severe symptoms and complications.
SymptomsThe more common symptoms of mumps are:
* Swelling of the parotid gland (or parotitis) in >90% of patients.
* Fever
* Headache
* Sore throat
* Orchitis, referring to painful inflammation of the testicle (see also PMID 2219620).
Signs and testsA physical examination confirms the presence of the swollen glands. Usually the disease is diagnosed on clinical grounds and no confirmatory laboratory testing is needed. If there is uncertainty about the diagnosis, serology or a saliva test for the virus may be carried out.
TreatmentThere is no specific treatment for mumps. Symptoms may be relieved by the application of intermittent ice or heat to the affected neck area, acetaminophen (paracetamol) for pain relief (aspirin is discouraged in children with a viral illness because of the risk of Reye's syndrome). Warm salt water gargles, soft foods, and extra fluids may also help relieve symptoms.
Patients are advised to avoid fruit juice or any acidic foods, since these stimulate the salivary glands, which can be painful.
PrognosisThe disease is self-limiting, and general outcome is good, even if other organs are involved. Sterility in men from involvement of the testes is very rare. After the illness, life-long immunity to mumps generally occurs.
ComplicationsKnown complications of mumps include:
* Infection of other organ systems
* Sterility in men (this is quite rare, and mostly occurs in older men)
* Mild forms of meningitis (rare, 40% of cases occur without parotid swelling)
* Encephalitis (very rare, rarely fatal)
* Profound (91 dB or more) but rare sensorineural hearing loss, uni- or bilateral
PreventionThe most common preventative measure against mumps is the MMR immunization (vaccine). This not only protects against mumps, but also protects against measles and rubella. The WHO recommends the use of mumps vaccines in all countries with well-functioning childhood vaccination programmes. In the United Kingdom it is routinely given to children at age 15 months. The American Academy of Pediatrics recommends the routine administration of MMR vaccine at ages 12-15 months and 4-6 years.The vaccination is repeated in some locations between 4 to 6 years of age, or between 11 and 12 years of age if not previously given. Efficacy of the vaccine depends on the strain of the vaccine, but is usually around 80%.
Some anti-vaccine activists protest against the administration of a vaccine against mumps, claiming that the attenuated vaccine strain is harmful, and/or that the wild disease is beneficial. Disagreeing, the WHO, the American Academy of Pediatrics, the Advisory Committee on Immunization Practices of the Centers for Disease Control and Prevention, the American Academy of Family Physicians, the British Medical Association and the Royal Pharmaceutical Society of Great Britain currently recommend routine vaccination of children against mumps. The British Medical Association and Royal Pharmaceutical Society of Great Britain had previously recommended against general mumps vaccination, changing that recommendation in 1987. In 1988 it became United Kingdom government policy to introduce mass child mumps vaccination programmes with the MMR vaccine, and MMR vaccine is now routinely administered in the UK.
Before the introduction of the mumps vaccine, the mumps virus was the leading cause of viral meningoencephalitis in the United States. However, encephalitis occurs rarely (less than 2 per 100,000 (Atkinson W, Humiston S, Wolfe C, Nelson R Editors. Epidemiology and Prevention of Vaccine-Preventable Diseases, 5th Edition, Centers for Disease Control and prevention.) In one of the largest studies in the literature, the most common symptoms of mumps meningoencephalitis were found to be fever (97%), vomiting (94%) and headache (88.8%). The mumps vaccine was introduced into the United States in December 1967: since its introduction there has been a steady decrease in the incidence of mumps and mumps virus infection. There were 152,209 cases of mumps reported in 1968; in 1998 there were only 666 cases reported.
RHEUMATIC FEVERRheumatic fever is an inflammatory disease which may develop after a Group A streptococcal infection (such as strep throat or scarlet fever) and can involve the heart, joints, skin, and brain.
General informationRheumatic fever is common worldwide and is responsible for many cases of damaged heart valves. In the Western countries, it became fairly rare since the 1950's, possibly due to higher hygienic standards. While it is far less common in the United States since the beginning of the 20th century, there have been a few outbreaks since the 1980s. Although the disease seldom occurs, it is serious and has a mortality of 2 - 5%.
Rheumatic fever primarily affects children between ages six and 15 and occurs approximately 20 days after strep throat or scarlet fever. In up to a third of cases, the underlying strep infection may not have caused any symptoms.
The rate of development of rheumatic fever in individuals with untreated strep infection is estimated to be 3 %. The rate of development is far lower in individuals who have received antibiotic treatment. Persons who have suffered a case of rheumatic fever have a tendency to develop flare-ups with repeated strep infections.
The recurrence of rheumatic fever is relatively common in the absence of maintenance of low dose antibiotics, especially during the first three to five years after the first episode of rheumatic fever. Heart complications may be long-term and severe, particularly if the happy happy heart valves are involved.
Diagnosis: Modified Jones CriteriaT. Duckett Jones, MD first published these criteria in 1944. They have been periodically revised by the American Heart Association in collaboration with other groups. Two major criteria, or one major and two minor criteria, when there is also evidence of a previous strep infection support the diagnosis of rheumatic fever.
Major Criteria * Carditis: inflammation of the heart muscle which can manifest as congestive heart failure with shortness of breath, pericarditis with a rub, or a new heart murmur.
* Migratory polyarthritis: a temporary migrating inflammation of the large joints, usually starting in the legs and migrating upwards.
* Sydenham's chorea (St. Vitus' dance): a characteristic series of rapid movements without purpose of the face and arms. This can occur very late in the disease.
* Erythema marginatum: a long lasting rash that begins on the trunk or arms as macules and spread outward to form a snakelike ring while clearing in the middle. This rash never starts on the face and is made worse with heat.
* Subcutaneous nodules (a form of Aschoff bodies): painless, firm collections of collagen fibers on the back of the wrist, the outside elbow, and the front of the knees. These now occur infrequently.
Minor Criteria * Fever: temperature elevation
* Arthralgia: Joint pain without swelling
* Laboratory abnormalities: increased Erythrocyte sedimentation rate, increased C reactive protein, leukocytosis
* Electrocardiogram abnormalities: a prolonged PR interval
* Evidence of Group A Strep infection: positive culture for Group A Strep, elevated or rising Antistreptolysin O titre
Other Signs and Symptoms
* Abdominal pain
* Epistaxis
PathophysiologyRheumatic fever is an autoimmune disease which occurs after an untreated Group A streptococcal infection, typically a throat infection. The antibodies formed against the bacteria attack parts of the body, typically the joints and the heart. This occurs because the streptoccal M antigen can stimulate B cells which are cross reactive with cardiac myosin.
Group A Streptococcus pyogenes has a cell wall that is composed of branched polymers which sometimes contain "M proteins" which are highly antigenic. The antibodies formed against these proteins sometimes cross-react with normal tissue causing damage. Depending on the site of damage, this can lead to the clinical symptoms described above.
TreatmentThe management of acute rheumatic fever is geared toward the reduction of inflammation with anti-inflammatory medications such as aspirin or corticosteroids. Individuals with positive cultures for strep throat should also be treated with antibiotics. Another important cornerstone in treating rheumatic fever includes the continuous use of low dose antibiotics (such as penicillin, sulfadiazine, or erythromycin) to prevent recurrence.
InfectionPatients with positive cultures for Streptococcus pyogenes should be treated with Penicillin as long as allergy is not present. This treatment will not alter the course of the acute disease.
InflammationPatients with significant symptoms may require corticosteroids. Salicylates are useful for pain.
Heart failureSome patients develop significant carditis which manifests as congestive heart failure. This requires the usual treatment for heart failure: diuretics, digoxin, etcetera. Unlike normal heart failure, rheumatic heart failure responds well to corticosteroids.
PreventionPrevention of recurrence is achieved by eradicating the acute infection and prophylaxis with antibiotics. The American Heart Association recommends prophylaxis continue at least 10 years.
RUBELLARubella (also known as epidemic roseola, German measles, liberty measles or three-day measles) is a disease caused by the Rubella virus. It is often mild and an attack can pass unnoticed. However, this can make the virus difficult to diagnose. The virus usually enters the body through the nose or throat. The disease can last 1-5 days. Children recover more quickly than adults. Like most viruses living along the respiratory tract, it is passed from person to person by tiny droplets in the air that are breathed out. Rubella can also be transmitted from a mother to her developing baby through the bloodstream via the placenta. The virus has an incubation period of 2 to 3 weeks during which it becomes established.
The name German measles has nothing to do with Germany. It comes from the Latin germanus, meaning "similar", since rubella and measles share many symptoms.
SymptomsSymptoms of rubella include:
* swollen glands or lymph nodes (may persist for up to a week)
* fever (rarely rises above 38 degrees Celsius [100.4 degrees Fahrenheit])
* rash (Appears on the face and then spreads to the trunk and limbs. It appears as pink dots under the skin. It appears on the first or third day of the illness but it disappears after a few days with no staining or peeling of the skin)
* Forchheimer's sign occurs in 20% of cases, and is characterized by small, red papules on the area of the soft palate
* flaking, dry skin
* inflammation of the eyes
* nasal congestion
* joint pain and swelling
* pain in the testicles
* loss of appetite
* headache
* nerves become weak or numb (very rare)
RisksRubella can affect anyone of any age and is generally a mild disease. However, rubella can cause congenital rubella syndrome in the fetus of an infected pregnant woman.
Prevention and treatmentSymptoms are usually treated with acetaminophen until the disease has run its course. There is no treatment available for congenital rubella.
Fewer cases of rubella occur since a vaccine became available in 1969, although decreased uptake of the MMR vaccine (e.g. in the UK) is expected to lead to a rise in incidence. In most Western countries, the vast majority of people are vaccinated against rubella as children at 12 to 15 months of age. A second dose is required before age 11. The vaccine gives lifelong protection against rubella. A side-effect of the vaccine can be transient arthritis.
The immunization program has been quite successful with Cuba declaring the disease eradicated in the 1990s and the United States eradicating it in 2005. Every minister of health in the Americas plans to eliminate the disease by 2010.
PERTUSSIS (whooping cough)Pertussis, also known as "whooping cough", is a highly contagious disease that is one of the leading causes of vaccine-preventable deaths. There are 30–50 million cases per year, and about 300,000 deaths per year. Most deaths occur in children under one year of age. Ninety percent of all cases occur in developing countries. It is caused by certain species of the bacterium Bordetella—usually B. pertussis, but some cases are caused by B. parapertussis.
The disease was recognizably described as early as 1578 by Guillaume de Baillou (1538-1616), but earlier reports date back at least to the 12th century. B. pertussis was isolated in pure culture in 1906 by Jules Bordet and Octave Gengou. The complete B. pertussis genome of 4,086,186 base pairs was sequenced in 2002.
CharacterizationThe disease is characterized initially by mild respiratory infections symptoms such as cough, sneezing, and runny nose (catarrhal stage). After one to two weeks the cough changes character, with paroxysms of coughing followed by an inspiratory "whooping" sound (paroxysmal stage). Coughing fits may be followed by vomiting not necessarily due to nausea but due to the sheer violence of the fit itself, which in severe cases leads to malnutrition. The fits, that do occur on their own, can also be triggered by yawning, stretching, laughing, or yelling. Coughing fits gradually diminish over one to two months. Other complications of the disease include pneumonia, encephalitis, pulmonary hypertension, and secondary bacterial superinfection.
TransmissionThe disease is spread by contact with airborne discharges from the mucous membranes of infected people. Laboratory diagnosis include; Calcium alginate throat swab, culture on Bordet-Gengou medium, immunofluorescence and serological methods. Treatment of the disease with antibiotics (often erythromycin, azithromycin, clarithromycin or trimethoprim-sulfamethoxazole) results in the person becoming less infectious but probably does not significantly alter the outcome of the disease. Close contacts who receive appropriate antibiotics, "chemoprophylaxis", during the 7–21 day incubation period may be protected from developing symptomatic disease.
VaccinesPertussis vaccines were initially formulated in 1926—most notable by Dr. Louis W. Sauer of Northwestern University and Evanston Hospital—as whole-cell preparations, but are now available as acellular preparations, which cause fewer side effects. They offer protection for only a few years, and are given so that immunity lasts through childhood, the time of greatest exposure and greatest risk. The immunizations are often given in combination with tetanus and diphtheria immunizations, at ages 2, 4, and 6 months, and later at 15–18 months and 4–6 years. Traditionally, pertussis vaccines are not given after age seven, as the frequency of side effects associated with the immunization tends to increase with age. The most serious side-effects of immunization are neurological: they include seizures and hypotonic episodes. An acellular vaccine preparation for older individuals is available in Canada and Europe, and two such products are being evaluated for their safety in adolescents and adults in the United States; a Food and Drug Administration decision was approved for use of the vaccine for 11-64 year olds in August 2005.
Other notesThe disease is much milder in adults than in children and many cases go undiagnosed or misdiagnosed. People may suffer from B. pertussis infection more than once in their life.
This disease is one of several that ravaged Native American populations after Europeans colonized the New World.
The Chinese call this disease the '100 Days Cough' due to the length that it lasts among most people.
Bordetella pertussis elaborates several virulence factors, including: pertussis toxin, an adenylate cyclase toxin, filamentous hemagglutinin, a tracheal cytotoxin, fimbriae, and pertactin.
FIFTH DISEASEFifth disease is also referred to as erythema infectiosum (meaning infectious redness) and as slapped cheek syndrome, slap face or slapped face.
In 1975 its cause was discovered to be Parvovirus B19.
The bright red cheeks are a defining symptom of the infection in children (hence the name "slapped cheek disease"), but the rash will not extend over the bridge of the nose or around the mouth. In addition to the red cheeks, children often develop a red, lacy rash on the rest of the body, with the upper arms and legs being the most common locations. Teenagers and adults may present with a self-limited arthritis.
Patients are usually no longer infectious once the characteristic rash of this disease has appeared. Any age may be affected although it is most common in children aged six to ten years. By the time adulthood is reached about half the population will have become immune following infection at some time in their past. Outbreaks can arise especially in nurseries and schools.
The disease is usually mild, but it does have the ability to cause some serious problems: it is associated with spontaneous abortion in pregnant women, and with transient aplastic crisis in persons with chronic hemolytic anemia. Primary infection in the first trimester has been linked to hydrops fetalis. The rash can last a couple of weeks and may itch.
The name fifth disease stems from the fact that when diseases causing childhood rashes were enumerated, it was the fifth listed.
