«Child’s» drop infections in adults. Meningococcal infection. Urgent states at the patients with infectious diseases with the droplet mechanism of transmission.
http://intranet.tdmu.edu.ua/data/books/And-INF.pdf
Rubella
Fig.1. Rubella
Rubella, commonly known as German measles, is a disease caused by the rubella virus. The name “rubella” is derived from the Latin, meaning little red. Rubella is also known as German measles because the disease was first described by German physicians in the mid-eighteenth century. This disease is often mild and attacks often pass unnoticed. The disease can last one to three days. Children recover more quickly than adults. Infection of the mother by Rubella virus during pregnancy can be serious; if the mother is infected within the first 20 weeks of pregnancy, the child may be born with congenital rubella syndrome (CRS), which entails a range of serious incurable illnesses. Spontaneous abortion occurs in up to 20% of cases.
Rubella is a common childhood infection usually with minimal systemic upset although transient arthropathy may occur in adults. Serious complications are very rare. Apart from the effects of transplacental infection on the developing fetus, rubella is a relatively trivial infection.
Acquired (i.e. not congenital) rubella is transmitted via airborne droplet emission from the upper respiratory tract of active cases. The virus may also be present in the urine, feces and on the skin. There is no carrier state: the reservoir exists entirely in active human cases. The disease has an incubation period of 2 to 3 weeks.’
In most people the virus is rapidly eliminated. However, it may persist for some months post partum in infants surviving the CRS. These children are a significant source of infection to other infants and, more importantly, to pregnant female contacts.
http://www.cdc.gov/Features/Rubella/
http://www.cdc.gov/Features/Rubella/
It should not be confused with rubeola, which was a historical name for measles.
Signs and symptoms
After an incubation period of 14–21 days, the primary symptom of rubella virus infection is the appearance of a rash (exanthem) on the face which spreads to the trunk and limbs and usually fades after three days. Other symptoms include low grade fever, swollen glands (post cervical lymphadenopathy), joint pains, headache and conjunctivitis. The swollen glands or lymph nodes can persist for up to a week and the fever rarely rises above 38 oC (100.4 oF). The rash 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.
Rubella can affect anyone of any age and is generally a mild disease, rare in infants or those over the age of 40. The older the person is the more severe the symptoms are likely to be. Up to one-third of older girls or women experience joint pain or arthritic type symptoms with rubella. The virus is contracted through the respiratory tract and has an incubation period of 2 to 3 weeks. During this incubation period, the carrier is contagious but may show no symptoms.
Congenital rubella syndrome
Main article: Congenital rubella syndrome
Rubella can cause congenital rubella syndrome in the newly born. The syndrome (CRS) follows intrauterine infection by Rubella virus and comprises cardiac, cerebral, ophthalmic and auditory defects. It may also cause prematurity, low birth weight, and neonatal thrombocytopenia, anaemia and hepatitis. The risk of major defects or organogenesis is highest for infection in the first trimester. CRS is the main reason a vaccine for rubella was developed. Many mothers who contract rubella within the first critical trimester either have a miscarriage or a still born baby. If the baby survives the infection, it can be born with severe heart disorders (PDA being the most common), blindness, deafness, or other life threatening organ disorders. The skin manifestations are called “blueberry muffin lesions.”
http://emedicine.medscape.com/article/968523-clinical#showall
Cause
Main article: Rubella virus
The disease is caused by Rubella virus, a togavirus that is enveloped and has a single-stranded RNA genome. The virus is transmitted by the respiratory route and replicates in the nasopharynx and lymph nodes. The virus is found in the blood 5 to 7 days after infection and spreads throughout the body. It is capable of crossing the placenta and infecting the fetus where it stops cells from developing or destroys them.
Increased susceptibility to infection might be inherited as there is some indication that HLA-A1 or factors surrounding A1 on extended haplotypes are be involved in virus infection or non-resolution of the disease.
Diagnosis of acquired rubella
Rubella virus specific IgM antibodies are present in people recently infected by Rubella virus but these antibodies can persist for over a year and a positive test result needs to be interpreted with caution. The presence of these antibodies along with, or a short time after, the characteristic rash confirms the diagnosis.
Prevention
Main article: MMR vaccine
Rubella infections are prevented by active immunisation programs using live, disabled virus vaccines. Two live attenuated virus vaccines, RA 27/3 and Cendehill strains, were effective in the prevention of adult disease. However their use in prepubertile females did not produce a significant fall in the overall incidence rate of CRS in the UK. Reductions were only achieved by immunisation of all children.
The vaccine is now given as part of the MMR vaccine. The WHO recommends the first dose is given at 12 to 18 months of age with a second dose at 36 months. Pregnant women are usually tested for immunity to rubella early on. Women found to be susceptible are not vaccinated until after the baby is born because the vaccine contains live virus.
The immunization program has been quite successful. Cuba declared the disease eliminated in the 1990s, and in 2004 the Centers for Disease Control and Prevention announced that both the congenital and acquired forms of rubella had been eliminated from the United States.
Treatment
There is no specific treatment for Rubella; management is a matter of responding to symptoms to diminish discomfort. Treatment of newly born babies is focused on management of the complications. Congenital heart defects and cataracts can be corrected by surgery. Management for ocular CRS is similar to that for age-related macular degeneration, including counseling, regular monitoring, and the provision of low vision devices, if required.
Prognosis
Rubella infection of children and adults is usually mild, self-limiting and often asymptomatic. The prognosis in children born with CRS is poor.
Epidemiology
Rubella is a disease that occurs worldwide. The virus tends to peak during the spring in countries with temperate climates. Before the vaccine to rubella was introduced in 1969, widespread outbreaks usually occurred every 6–9 years in the United States and 3–5 years in Europe, mostly affecting children in the 5-9 year old age group. Since the introduction of vaccine, occurrences have become rare in those countries with high uptake rates. However, in the UK there remains a large population of men susceptible to rubella who have not been vaccinated. Outbreaks of rubella occurred amongst many young men in the UK in 1993 and in 1996 the infection was transmitted to pregnant women, many of whom were immigrants and were susceptible. Outbreaks still arise, usually in developing countries where the vaccine is not as accessible.
During the epidemic in the US between 1962-1965, Rubella virus infections during pregnancy were estimated to have caused 30,000 still births and 20,000 children to be born impaired or disabled as a result of CRS. Universal immunisation producing a high level of herd immunity is important in the control of epidemics of rubella.
Measles
Fig.2. Measles
Fig.3. Measles virus
Measles, also known as rubeola, is one of the most contagious infectious diseases, with at least a 90% secondary infection rate in susceptible domestic contacts. It can affect people of all ages, despite being considered primarily a childhood illness. Measles is marked by prodromal fever, cough, coryza, conjunctivitis, and pathognomonic enanthem (ie, Koplik spots), followed by an erythematous maculopapular rash on the third to seventh day. Infection confers life-long immunity.
A generalized immunosuppression that follows acute measles frequently predisposes patients to bacterial otitis media and bronchopneumonia. In approximately 0.1% of cases, measles causes acute encephalitis. Subacute sclerosing panencephalitis (SSPE) is a rare chronic degenerative disease that occurs several years after measles infection.
After an effective measles vaccine was introduced in 1963, the incidence of measles decreased significantly. Nevertheless, measles remains a common disease in certain regions and continues to account for nearly 50% of the 1.6 million deaths caused each year by vaccine-preventable childhood diseases. The incidence of measles in the United States and worldwide is increasing, with outbreaks being reported particularly in populations with low vaccination rates.
Maternal antibodies play a significant role in protection against infection in infants younger than 1 year and may interfere with live-attenuated measles vaccination. A single dose of measles vaccine administered to a child older than 12 months induces protective immunity in 95% of recipients. Because measles virus is highly contagious, a 5% susceptible population is sufficient to sustain periodic outbreaks in otherwise highly vaccinated populations.
A second dose of vaccine, now recommended for all school-aged children in the United States, induces immunity in about 95% of the 5% who do not respond to the first dose. Slight genotypic variation in recently circulating strains has not affected the protective efficacy of live-attenuated measles vaccines.
Unsubstantiated claims that suggest an association between the measles vaccine and autism have resulted in reduced vaccine use and contributed to a recent resurgence of measles in countries where immunization rates have fallen to below the level needed to maintain herd immunity.
Considering that for industrialized countries such as the United States, endemic transmission of measles may be reestablished if measles immunity falls to less than 93-95%, efforts to ensure high immunization rates among people in both developed and developing countries must be sustained.
Supportive care is normally all that is required for patients with measles. Vitamin A supplementation during acute measles significantly reduces risks of morbidity and mortality.
For patient education resources, see Bacterial and Viral Infections, as well as Measles and Skin Rashes in Children.
History
The patient history is notable for exposure to the virus. The incubation period from exposure to onset of measles symptoms ranges from 7 to 14 days (average, 10-12 days). Patients are contagious from 1-2 days before the onset of symptoms. Healthy children are also contagious during the period from 3-5 days before the appearance of the rash to 4 days after the onset of rash. On the other hand, immunocompromised individuals can be contagious during the duration of the illness.
The first sign of measles is usually a high fever (often >104o F [40o C]) that typically lasts 4-7 days. This prodromal phase is marked by malaise, fever, anorexia, and the classic triad of conjunctivitis (see the image below), cough, and coryza (the “3 Cs”). Other possible associated symptoms include photophobia, periorbital edema, and myalgias.
Measles conjunctivitis
The characteristic enanthem generally appears 2-4 days after the onset of the prodrome and lasts 3-5 days. Small spots (Koplik spots) can be seen inside the cheeks during this early stage (see the image below).
Koplik spots in measles.
The exanthem usually appears 1-2 days after the appearance of Koplik spots; mild pruritus may be associated. On average, the rash develops about 14 days after exposure, starting on the face and upper neck (see the image below) and spreading to the extremities. Immunocompromised patients may not develop a rash.
Child with measles.
The entire course of uncomplicated measles, from late prodrome to resolution of fever and rash, is 7-10 days. Cough may be the final symptom to appear.
Modified and atypical measles
Modified measles is a milder form of measles that occurs in individuals who have received serum immunoglobulin after their exposure to the measles virus. Similar but milder symptoms and signs may still occur, but the incubation period may be as long as 21 days.
Atypical measles occurs in individuals who were vaccinated with the original killed-virus measles vaccine between 1963 and 1967 and who have incomplete immunity. After exposure to the measles virus, a mild or subclinical prodrome of fever, headache, abdominal pain, and myalgias precedes a rash that begins on the hands and feet and spreads centripetally. The eruption is accentuated in the skin folds and may be macular, vesicular, petechial, or urticarial. The live-attenuated vaccine replaced the killed vaccine in 1967 and is not associated with atypical measles.
Measles (IPA: /mizəlz/) is an infection of the respiratory system caused by a virus, specifically a paramyxovirus of the genus Morbillivirus. Morbilliviruses, like other paramyxoviruses, are enveloped, single-stranded, negative-sense RNA viruses. Symptoms include fever, cough, runny nose, red eyes and a generalized, maculopapular, erythematous rash.
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. The infection has an average incubation period of 14 days (range 6–19 days) and infectivity lasts from 2–4 days prior to 2–5 days following the onset of the rash.
Measles was historically called rubeola. In contrast, German measles is an unrelated condition caused by the rubella virus.
Signs and symptoms
Fig.4. This patient presented on the third pre-eruptive day with “Koplik spots” indicative of the beginning onset of measles.
The classical symptoms of measles include four day fevers, the three Cs—cough, coryza (runny nose) and conjunctivitis (red eyes). The fever may reach up to 40° Celsius (104° Fahrenheit). Koplik’s spots seen inside the mouth are pathognomonic (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 characteristic measles rash is classically described as a generalized, maculopapular, erythematous rash that begins several days after the fever starts. It starts on the head before spreading to cover most of the body, often causing itching. The rash is said to “stain”, changing colour from red to dark brown, before disappearing.
Complications
Complications with measles are relatively common, ranging from relatively mild and less serious diarrhea, to pneumonia and encephalitis (subacute sclerosing panencephalitis), corneal ulceration leading to corneal scarring. Complications are usually more severe amongst adults who catch the virus.
Most complications of measles occur because the measles virus suppresses the host’s immune responses, resulting in a reactivation of latent infections or superinfection by a bacterial pathogen. Consequently, pneumonia, whether due to the measles virus itself, to tuberculosis, to or another bacterial etiology, is the most frequent complication. Pleural effusion, hilar lymphadenopathy, hepatosplenomegaly, hyperesthesia, and paresthesia may also be noted.
Complications of measles are more likely to occur in persons younger than 5 years or older than 20 years, and complication rates are increased in persons with immune deficiency disorders, malnutrition, vitamin A deficiency, and inadequate vaccination. Immunocompromised children and adults are at increased risk for severe infections and superinfections.
Common infectious complications include otitis media, interstitial pneumonitis,[19] bronchopneumonia, laryngotracheobronchitis (ie, croup), exacerbation of tuberculosis, transient loss of hypersensitivity reaction to tuberculin skin test, encephalomyelitis, diarrhea, sinusitis, stomatitis, subclinical hepatitis, lymphadenitis, and keratitis, which can lead to blindness. In fact, measles remains a common cause of blindness in many developing countries.
Rare complications include hemorrhagic measles, purpura fulminans, hepatitis, disseminated intravascular coagulation (DIC), subacute sclerosing panencephalitis (SSPE), thrombocytopenia, appendicitis, ileocolitis, pericarditis, myocarditis, acute pancreatitis, and hypocalcemia. Transient hepatitis may occur during an acute infection.
Approximately 1 of every 1,000 patients develops acute encephalitis, which often results in permanent brain damage and is fatal in about 10% of patients. In children with lymphoid malignant diseases, delayed-acute measles encephalitis may develop 1-6 months after the acute infection and is generally fatal.
An even rarer complication is SSPE, a degenerative CNS disease that can result from a persistent measles infection. SSPE is characterized by the onset of behavioral and intellectual deterioration and seizures years after an acute infection (the mean incubation period for SSPE is approximately 10.8 years).
The complications of measles in the pregnant mother include pneumonitis, hepatitis, subacute sclerosing panencephalitis, premature labor, spontaneous abortion, and preterm birth of the fetus. Perinatal transmission rates are low.
The fatality rate from measles for otherwise healthy people in developed countries is 3 deaths per thousand cases. In underdeveloped nations with high rates of malnutrition and poor healthcare, fatality rates have been as high as 28%. In immunocompromised patients (e.g. people with AIDS) the fatality rate is approximately 30 percent.
Cause
The measles virus is a highly contagious airborne pathogen which spreads primarily via the respiratory system. The virus is transmitted in respiratory secretions, and can be passed from person to person via aerosol droplets containing virus particles, such as those produced by a coughing patient. Once transmission occurs, the virus infects and replicates in the lymphatic system, urinary tract, conjunctivae, blood vessels and central nervous system of its new host. The role of epithelial cells is uncertain, but the virus must infect them to spread to a new individual.
Patients with the measles should be placed on droplet precautions.
Humans are the only knowatural hosts of measles, although the virus can infect some non-human primate species.
Diagnosis
Clinical diagnosis of measles requires a history of fever of at least three days together with at least one of the three C’s (cough, coryza, conjunctivitis). 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. In cases of measles infection following secondary vaccine failure IgM antibody may not be present. However, in the rare case of a secondary vaccine failure, other external symptoms may be present, including nausea, headaches, or a feeling of slight dizziness when turning one’s head to the left. In these cases serological confirmation may be made by showing IgG antibody rises by enzyme immunoassay or complement fixation. In children, where phlebotomy is inappropriate, saliva can be collected for salivary measles specific IgA test. Adults ommended to seek medical help right away.
Positive contact with other patients known to have measles adds strong epidemiological evidence to the diagnosis. The contact with any infected person in any way, including semen through sex, saliva, or mucus can cause infection.
Histologically, a unique cell can be found in the paracortical region of hyperplastic lymph nodes in patients affected with this condition. This cell, known as the Warthin-Finkeldey cell, is a multinucleated giant with eosinophilic cytoplasmic and nuclear inclusions.
Although the diagnosis of measles is usually determined from the classic clinical picture (see Clinical), laboratory identification and confirmation of the diagnosis are necessary for the purposes of public health and outbreak control. Laboratory confirmation is achieved by means of serologic testing for immunoglobulin G (IgG) and M (IgM) antibodies, isolation of the virus, and reverse-transcriptase polymerase chain reaction (RT-PCR) evaluation.
A complete blood cell count (CBC) may reveal leukopenia with a relative lymphocytosis and thrombocytopenia. Liver function test (LFT) results may reveal elevated transaminase levels in patients with measles hepatitis.
Consult public health or infectious disease specialists for recommendations and guidelines for diagnostic confirmation of cases and prophylaxis of susceptible contacts.
Case reporting
Because the transmission of indigenous measles has been interrupted in the United States and all recent US epidemics have been linked to imported cases, immediately reporting any suspected case of measles to a local or state health department is imperative, as is obtaining serum for IgM antibody testing as soon as possible (ie, on or after the third day of rash).
The US Centers for Disease Control and Prevention (CDC) clinical case definition for reporting purposes requires only the following:
- Generalized rash lasting 3 days or longer
- Temperature of 101.0°F (38.3°C) or higher
- Cough, coryza, or conjunctivitis
Further, for reporting purposes for the CDC, cases are classified as follows:
- Suspected – Any febrile illness accompanied by rash
- Probable – A case that meets the clinical case definition, has noncontributory or no serologic or virologic testing, and is not epidemiologically linked to a confirmed case
- Confirmed – A case that is laboratory confirmed or that meets the clinical case definition and is epidemiologically linked to a confirmed case; a laboratory-confirmed case need not meet the clinical case definition
Prevention
In developed countries, most children are immunized against measles by 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 second dose is usually given to children between the ages of four and five, in order to increase rates of immunity. Vaccination rates have been high enough to make measles relatively uncommon. Even a single case in a college dormitory 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 where measles is highly endemic, the WHO recommend that two doses of vaccine be given at six months and at nine months of age. The vaccine should be given whether the child is HIV-infected or not. The vaccine is less effective in HIV-infected infants, but the risk of adverse reactions is low.
Unvaccinated populations are at risk for the disease. After vaccination rates dropped in northern Nigeria in the early 2000s due to religious and political objections, the number of cases rose significantly, and hundreds of children died. A 2005 measles outbreak in Indiana was attributed to children whose parents refused vaccination.[10] In the early 2000s the MMR vaccine controversy in the United Kingdom regarding a potential link between the combined MMR vaccine (vaccinating children from mumps, measles and rubella) and autism prompted a reemergence of the “measles party”, where parents deliberately expose their child to measles in the hope of building up the child’s immunity without an injection. This practice poses many health risks to the child, and has been discouraged by the public health authorities. Scientific evidence provides no support for the hypothesis that MMR plays a role in causing autism. However, the MMR scare in Britain caused uptake of the vaccine to plunge, and measles cases came back: 2007 saw 971 cases in England and Wales, the biggest rise in occurrence in measles cases since records began in 1995.
The joint press release by members of the Measles Initiative brings to light another benefit of the fight against measles: “Measles vaccination campaigns are contributing to the reduction of child deaths from other causes. They have become a channel for the delivery of other life-saving interventions, such as bed nets to protect against malaria, de-worming medicine and vitamin A supplements. Combining measles immunization with other health interventions is a contribution to the achievement of Millennium Development Goal Number 4: a two-thirds reduction in child deaths between 1990 and 2015.”
Treatment
There is no cure for measles. Most patients with uncomplicated measles will recover with rest and supportive treatment.
Some patients will develop pneumonia as a sequela to the measles.
Epidemiology
According to the World Health Organization (WHO), measles is a leading cause of vaccine-preventable childhood mortality. Worldwide, the fatality rate has been significantly reduced by partners in the Measles Initiative: the American Red Cross, the United States Centers for Disease Control and Prevention (CDC), the United Nations Foundation, UNICEF and the World Health Organization (WHO). Globally, measles deaths are down 60 percent, from an estimated 873,000 deaths in 1999 to 345,000 in 2005. Africa has seen the most success, with annual measles deaths falling by 75 percent in just 5 years, from an estimated 506,000 to 126,000.
History and culture
The Antonine Plague, 165-180 AD, also known as the Plague of Galen, who described it, was probably smallpox or measles. Disease killed as much as one-third of the population in some areas, and decimated the Roman army. The first scientific description of measles and its distinction from smallpox and chickenpox is credited to the Persian physician, Muhammad ibn Zakariya ar-Razi (860-932), known to the West as “Rhazes”, who published a book entitled The Book of Smallpox and Measles (in Arabic: Kitab fi al-jadari wa-al-hasbah).
Measles is an endemic disease, meaning that it has been continually present in a community, and many people develop resistance. In populations that have not been exposed to measles, exposure to a new disease can be devastating. In 1529, a measles outbreak in Cuba killed two-thirds of the natives who had previously survived smallpox. Two years later measles was responsible for the deaths of half the population of Honduras, and had ravaged Mexico, Central America, and the Inca civilization.
In roughly the last 150 years, measles has been estimated to have killed about 200 million people worldwide. During the 1850s, measles killed a fifth of Hawaii‘s people. In 1875, measles killed over 40,000 Fijians, approximately one-third of the population. In the 19th century, the disease decimated the Andamanese population. In 1954, the virus causing the disease was isolated from an 11-year old boy from the United States, David Edmonston, and adapted and propagated on chick embryo tissue culture.[22] To date, 21 strains of the measles virus have been identified. Licensed vaccines to prevent the disease became available in 1963.
Fig.6. Intra oral rash of measles
Fig.7. Measles in African Child
Fig.8. Measles. This child shows a day-4 rash with measles
Fig.9. Histopathology of measles pneumonia. Giant cell
Mumps
Fig.10. Mumps
Mumps or epidemic parotitis is a viral disease of the human species, caused by the mumps virus. Prior to the development of vaccination and the introduction of a vaccine, it was a common childhood disease worldwide, and is still a significant threat to health in the third world.
Painful swelling of the salivary glands (classically the parotid gland) is the most typical presentation. Painful testicular swelling (orchitis) and rash may also occur. The symptoms are generally not severe in children. In teenage males and men, complications such as infertility or subfertility are more common, although still rare in absolute terms. The disease is generally self-limited, running its course before receding, with no specific treatment apart from controlling the symptoms with painkillers.
Symptoms
Fig.11. Comparison of a person before and after contracting the mumps
The more common symptoms of mumps are:
· Parotid inflammation (or parotitis) in 60–70% of infections and 95% of patients with symptoms. Parotitis causes swelling and local pain, particularly when chewing. It can occur on one side (unilateral) but is more common on both sides (bilateral) in about 90% of cases.
· Fever
· Headache
· Orchitis, referring to painful inflammation of the testicle. Males past puberty who develop mumps have a 30 percent risk of orchitis.
Other symptoms of mumps can include dry mouth, sore face and/or ears and occasionally in more serious cases, loss of voice. In addition, up to 20% of persons infected with the mumps virus do not show symptoms, so it is possible to be infected and spread the virus without knowing it.
Prodrome
Fever and headache are prodromal symptoms of mumps, together with malaise and anorexia.
Signs and tests
A 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, a test of saliva, or blood may be carried out; a newer diagnostic confirmation, using real-time nested polymerase chain reaction (PCR) technology, has also been developed. An estimated 20%-30% of cases are asymptomatic. As with any inflammation of the salivary glands, serum amylase is often elevated.
Mumps is a contagious disease that is spread from person-to-person through contact with respiratory secretions such as saliva from an infected person. When an infected person coughs or sneezes, the droplets aerosolize and can enter the eyes, nose, or mouth of another person. Mumps can also be spread by sharing food, sharing drinks, and kissing. The virus can also survive on surfaces and then be spread after contact in a similar manner.
A person infected with mumps is contagious from approximately 6 days before the onset of symptoms until about 9 days after symptoms start. The incubation period (time until symptoms begin) can be from 14–25 days but is more typically 16–18 days.
There is no specific treatment for mumps. Symptoms may be relieved by the application of intermittent ice or heat to the affected neck area and by acetaminophen/paracetamol (Tylenol) for pain relief. Aspirin use is not used due to a hypothetical link with 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.
Death is very unusual. The disease is self-limiting, and general outcome is good, even if other organs are involved.
Known complications of mumps include:
· Infection of other organ systems
· Mumps viral infections in adolescent and adult males carry an up to 30% risk that the testes may become infected (orchitis or epididymitis), which can be quite painful; about half of these infections result in testicular atrophy, and in rare cases sterility can follow.
· Spontaneous abortion in about 27% of cases during the first trimester of pregnancy.
· Mild forms of meningitis in up to 10% of cases (40% of cases occur without parotid swelling)
· Oophoritis (inflammation of ovaries) in about 5% of adolescent and adult females, but fertility is rarely affected.
· Pancreatitis in about 4% of cases, manifesting as abdominal pain and vomiting
· Encephalitis (very rare, and fatal in about 1% of the cases when it occurs)
· Profound (91 dB or more) but rare sensorineural hearing loss, uni- or bilateral. Acute unilateral deafness occurs in about 0.005% of cases.
After the illness, life-long immunity to mumps generally occurs; reinfection is possible but tends to be mild and atypical.
The most common preventative measure against mumps is immunization with a mumps vaccine. The vaccine may be given separately or as part of the MMR immunization vaccine which also protects against measles and rubella. In the US, MMR is now being supplanted by MMRV, which adds protection against chickenpox. The WHO (World Health Organization) 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 at 4–6 years. In some locations, the vaccine is given again between 4 to 6 years of age, or between 11 and 12 years of age if not previously given. The efficacy of the vaccine depends on the strain of the vaccine, but is usually around 80%. The Jeryl Lynn strain is most commonly used in developed countries but has been shown to have reduced efficacy in epidemic situations. The Leningrad-Zagreb strain commonly used in developing countries appears to have superior efficacy in epidemic situations.
Due to the outbreaks within college and university settings, many governments have established vaccination programs to prevent large-scale outbreaks. In Canada, provincial governments and the Public Health Agency of Canada have all participated in awareness campaigns to encourage students ranging from grade 1 to college and university to get vaccinated.
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). 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 151,209 cases of mumps reported in 1968. Since 2001, the case average was only 265 per year, excluding an outbreak of >6000 cases in 2006 attributed largely to university contagion in young adults.
Etiology
Scarlet fever is a streptococcal disease. Streptococci are gram-positive cocci that grow in chains. They are classified by their ability to produce a zone of hemolysis on blood agar and by differences in carbohydrate cell wall components (A-H and K-T). They may be alpha-hemolytic (partial hemolysis), beta-hemolytic (complete hemolysis), or gamma-hemolytic (no hemolysis).
Group A streptococci are normal inhabitants of the nasopharynx. Group A streptococci can cause pharyngitis, skin infections (including erysipelas pyoderma and cellulitis), pneumonia, bacteremia, and lymphadenitis.
Most streptococci excrete hemolyzing enzymes and toxins. The erythrogenic toxins produced by GABHS are the cause of the rash of scarlet fever. The erythema-producing toxin was discovered by Dick and Dick in 1924. Scarlet fever is usually associated with pharyngitis; however, in rare cases, it follows streptococcal infections at other sites.
Although infections may occur year-round, the incidence of pharyngeal disease is highest in school-aged children (5-15 y) during winter and spring and in a setting of crowding and close contact. Person-to-person spread by means of respiratory droplets is the most common mode of transmission. It can rarely be spread through contaminated food, as seen in a recent outbreak in China.
The organism is able to survive extremes of temperature and humidity, which allows spread by fomites. Geographic distribution of skin infections tends to favor warmer or tropical climates and occurs mainly in summer or early fall in temperate climates.
The incubation period for scarlet fever ranges from 12 hours to 7 days. Patients are contagious during the acute illness and during the subclinical phase.
Scarlet fever is a disease caused by an erythrogenic exotoxin released by Streptococcus pyogenes. The term Scarlatina may be used interchangeably with Scarlet Fever, though it is commonly used to indicate the less acute form of Scarlet Fever that is often seen since the beginning of the twentieth century.
It is characterized by:
· Sore throat
· Fever
· Bright red tongue with a “strawberry” appearance
· Characteristic rash, which:
· is fine, red, and rough-textured; it blanches upon pressure
· appears 12–48 hours after the fever
· generally starts on the chest, armpits, and behind the ears
· spares the face (although some circumoral pallor is characteristic)
· is worse in the skin folds. These are called Pastia lines (where the rash runs together in the arm pits and groins) appear and can persist after the rash is gone
· may spread to cover the uvula.
· The rash begins to fade three to four days after onset and desquamation (peeling) begins. “This phase begins with flakes peeling from the face. Peeling from the palms and around the fingers occurs about a week later.”[2] Peeling also occurs in axilla, groin, and tips of the fingers and toes.
Diagnosis of scarlet fever is clinical. The blood test shows marked leukocytosis with neutrophilia and conservated or increased eosinophils, high erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP), and elevation of antistreptolysin O titer. Blood culture is rarely positive, but the streptococci can usually be demonstrated in throat culture. The complications of scarlet fever include septic complications due to spread of streptococcus in blood and immune-mediated complications due to an aberrant immune response. Septic complications, today rare, include ear and sinus infection, streptococcal pneumonia, empyema thoracis, meningitis and full-blown sepsis, upon which the condition may be called malignant scarlet fever.
Immune complications include acute glomerulonephritis, rheumatic fever and erythema nodosum. The secondary scarlatinous disease, or secondary malignant syndrome of scarlet fever, includes renewed fever, renewed angina, septic ear, nose, and throat complications and kidney infection or rheumatic fever and is seen around the eighteenth day of untreated scarlet fever.
Fig.13. Scarlet Fever’s pebbly, dry rash.
The rash is the most striking sign of scarlet fever. It usually begins looking like a bad sunburn with tiny bumps, and it may itch. The rash usually appears first on the neck and face, often leaving a clear unaffected area around the mouth. It spreads to the chest and back, then to the rest of the body. In body creases, especially around the underarms and elbows, the rash forms classic red streaks (on very dark skin, the streaks may appear darker than the rest of the skin). Areas of rash usually turn white (or paler brown, with dark complected skin) when you press on them. By the sixth day of the infection the rash usually fades, but the affected skin may begin to peel.
Aside from the rash, there are usually other symptoms that help to confirm a diagnosis of scarlet fever, including a reddened sore throat, a fever at or above 101 °F (38.3 C), and swollen glands in the neck. Scarlet fever can also occur with a low fever. The tonsils and back of the throat may be covered with a whitish coating, or appear red, swollen, and dotted with whitish or yellowish specks of pus. Early in the infection, the tongue may have a whitish or yellowish coating. A person with scarlet fever also may have chills, body aches, nausea, vomiting, and loss of appetite.
When scarlet fever occurs because of a throat infection, the fever typically stops within 3 to 5 days, and the sore throat passes soon afterward. The scarlet fever rash usually fades on the sixth day after sore throat symptoms began, but skin that was covered by rash may begin to peel. This peeling may last 10 days. The infection itself is usually cured with a 10-day course of antibiotics, but it may take a few weeks for tonsils and swollen glands to return to normal.
In rare cases, scarlet fever may develop from a streptococcal skin infection like impetigo. In these cases, the person may not get a sore throat.
Husband and wife Gladys Henry Dick and George Frederick Dick developed a vaccine in the 1920s that was later eclipsed by penicillin in the 1940s. Other than the occurrence of the diarrhea, the treatment and course of scarlet fever are no different from those of any strep throat. In case of penicillin allergy, clindamycin or erythromycin can be used with success. Patients should no longer be infectious after taking antibiotics for 24 hours. Persons who have been exposed to scarlet fever should watch carefully for a full week for symptoms, especially if aged 3 to young adult. It’s very important to be tested (throat culture) and if positive, seek treatment. For reasons unknown, toddlers rarely contract scarlet fever.
MENINGOCOCCAL INFECTION
Definition
Meningococcal infection is an acute infectious disease of the human, caused by meningococcous Neisseria Meningitigis. The mechanism of the transmission of the infection is air-drop. The disease is characterized by damage of mucous membrane of nasopharynx (nasopharingitis), generalization of the process in form of specific septicemia (meningococcemia) and inflammation of the soft cerebral membranes (meningitis).
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History and geographical distribution
Epidemic cerebrospinal meningitis (one of the most clinically expressive forms of the disease) was known else in profound antiquity. The description of outbreaks of this infection is contained in reports of Areteus (III century of our era), Egynsky (VII century).
Epidemic cerebrospinal meningococcal meningitis was first described by Vieusseaux in 1805. Subsequent reports throughout the nineteenth century confirm its episodic epidemic nature with a propensity for affecting young children and military recruits assembled in stationary barrack situations. In 1887, Weichselbaum isolated the meningococcus from the cerebrospinal fluid, and the etiologic relationship between this organisms and epidemic meningitis was firmly established.
Kiefer in 1896 and Albrecht and Ghon in 1901 found that healthy persons could become carriers of the meningococcus. Serotypes of the meningococcus were first recognized by Dopter in 1909. This laid the basis for serum therapy in the treatment of meningococcal infection. The agent was isolated from the blood by V. Osler in 1899. It had an important meaning, because many problems of pathogenesis of the disease were explained. It was evidence that meningitis is not single manifestation of the disease.
In 1937, sulfonamide therapy radically altered the outcomes of meningococcal infection. With the advent of antibiotic agents, treatment of meningococcal infection became more effective, and mortality declined. With the subsequent world wide emergence of resistant strains and with the absence of effective chemoprophylaxis, renewed interest in immunoprevention has occurred and has led to the development of safe and effective vaccines against the groups A, C, Y and W-135 meningococcal group.
Meningococcal infection occurs on the all continents. It is serious problem for public health. It is registered in 170 countries of the world.
Etiology
The causative agent is Neisseria meningitidis. It is small gramm-negative diplococcus, aerobic, catalise and oxidase-positive, not-motile and possess a polysaccharide capsule, which is the main antigen and determines the serotype of the species. Meningococcus may be seen inside and outside of neutrophills (Fig.14). The main serogroups of pathogenic organisms are A, B, C, D, and W135, X, Y, Z and L. The bacterial membrane is a lipopolysaccaride.
Fig.14. Neisseria meningitidis
The pathogenic properties of meningococcus are known insufficiently, because meningococcal infection is anthroponosis. The factors of pathogenic action of meningococcus are biological properties, promoting its attachment on the mucous membrane of nasopharynx, depression symbiotic microflora, penetration through mucous barriers, toxic properties and other.
One of such properties is specific attachment or adhesion of meningococcous to the cells of epithelium of respiratory tract. Adhesion is phenomenon, promoting to colonization of meningococcus on the mucus. Physical factors (adsorption of microbes on the surface of the cell) and fermentative processes have the meaning in the appearance of adhesion.
Meningococci are very exacting to composition of nutritive mediums. Its reproduction may be only in presence of human’s protein or animal’s protein. Due to destruction of the microbe’s cell endotoxin is delivered (of lipopolysaccharide origin). Exotoxin is no produced. The agent of meningococcal infection is characterized by low resistance in the environment. Meningococci perish during temperature 50°C through 5 minutes, during temperature 100°C – through 30 seconds. Meningococci have a little resistance to low temperature.
Epidemiology
Meningococcal infection is typical anthroponosis. The sourses of infection are healthy carriers of meningococcus, the patients with meningococcal nasopharingitis and the patients with generalized forms of the disease.
The patients with generalized form are more dangerous. It is proved that they are dangerous for surrounding persons in 6 times than healthy carriers. However, the main sources of the infection are carriers, because 1200-1800 (according other data – 50000) carriers have occasion to one patients with generalized form of the disease.
Thus, the patients with generalized form of the disease are the source of infection for 1-3 % of infected persons, the patients with meningococcal nasopharingitis – for 10-30 %, carriers are the sources of infection for 70-80 % from general number of infected.
The level of healthy carriers promotes the level of morbility in certain region. So, carriers may compose 3-12 %. It is temperate sporadic morbility. Carriers may achieve 20 %. This situation is marked as unsatisfactory. The outbreaks are observed. Carriers may achieve 30-40 %. In this case epidemic of meningococcal infection arises.
The mechanism of transmission of the infection is air-drop. The infection is realized during cough, sneezing. In this the narrow contact and sufficient exposition are necessary. It is proved by A.A. Favorova (1976) that the infection is realized on the distance less 0,5 meter.
The wide distribution of meningococcal infection is promoted some causes in the countries of equatorial Africa. The main causes are connected with social factors (unsatisfactory sanitary-hygienic conditions of the life of the majority part of the population, high density of the population and other).
In meningococcal infection one of an important characteristic of epidemic process is periodical rise and fall of the morbidity. The duration of the period with high morbidity is different. It may be 5-10 years and more. Then the period of the fall of the morbidity becomes. It is continued from 5 till 20 years.
In meningococcal infection epidemic process is characterized by seasonal spread. It is manifested especially during epidemics. The morbidity may compose 60-70% from year’s morbidity during seasonal rise. The onset of the seasonal rise is in quanuary in the countries with temperate clinimate. It achieves of maximum in march – april.
The estimate of the age morbidity of meningococcal infection testifies about that 70-80 % of the cases of the diseases have occasion to children. Children of the age 1-5 years compose 50 %. Meningococcal infection is marked rarely at the first three month of the life.
The persons of the young age (15-30 years) compose the majority among adult patients. It is explained by social factors and features of the life young people (service in the army study in the educational establishments, living in the hostel). These factors explain predomination of men in the structure of the morbidity.
The age of carriers of meningococcal infection is different from the age of the patient. The larger part of carriers is reveled among adults. The portion of the children is a little. The morbidity is higher in the towns then rural locality.
The considerable outbreaks of the diseases were described in the educational establishments of the closed type and especially among military (as at peaceful time such as during war).
Pathogenesis
In meningococcal infection entrance gates are mucous membrane of nasopharynx. It is place of primary localization of the agent. Further meningococci may persist in epithelium of nasopharynx in majority of the cases. It is manifested by asymptomatic healthy carriers. In some cases meningococci may cause inflammation of mucous membrane of upper respiratory tract. It leads to development of nasopharingitis.
The localization of meningococcus on mucous membrane of nasopharynx leads to development of inflammation in 10-15 % of the cases.
The stages of inculcation on the mucous membrane of nasopharynx and penetration of meningococcus into the blood precede to entrance of endotoxin into the blood and cerebrospinal fluid. These stages are realized with help of factors of permeability. It promotes of the resistance of the meningococcus to phagocytosis and action antibodies.
Meningococci are able to break local barriers with help of factors of spread (hyaluronidase). Capsule protects meningococci from phagocytosis. Hematogenous way is the principal way of the spread of the agent in the organism (bacteremia, toxinemia). Only the agent with high virulence and invasive strains may penetrate through hematoencephalitic barrier. The strains of serogroup A high invasivicity.
Meningococci penetrate into the blood after break of protective barriers of mucous membrane of upper respiratory tract. There is hematogenous dissemination (meningococcemia). It is accompanied by massive destruction of the agents with liberation of endotoxin. Meningococcemia and toxinemia lead to damage of endothelium of the vessels. Hemorrhages are observed in mucous membrane, skin and parenchymatous organs. It may be septic course of meningococcemia with formation of the secondary metastatic focuses in the endocardium, joints, internal mediums of the eyes.
In most of the cases penetration of meningococci in the cerebrospinal fluid and the soft cerebral covering is fought about by hematogenous ways through the hematoencephalic barrier. Sometimes meningococci may penetrate into the skull through perineural, perilymphatic and the perivascular way of the olfactory tract, through the enthoid bone.
Thus the meningococci enter into subarachnoid space, multiply and course serous-purulent and purulent inflammation of the soft cerebral coverings. The inflammatory process is localized on the surface of the large craniocerebral hemispheres, and rarely, on the basis, but sometimes it may spread in the covering of the spinal cord. During severe duration of the inflammatory process the cranium is covered by purulent mather (so-cold “purulent cap”). It may lead to involvement of the brain’s matter into inflammatory process and meningoencephalitis.
The process may engulf the rootlets of – VII, VIII, V, VI, III and XII pairs of cranial nerves.
Pathogenic properties of the agent, state of macroorganism, state of immune system, functional state of hematoencephalitic barrier have the meaning in the appearance of meningitis of any etiology.
Endothelium of capillaries, basal membrane, “vascular pedicles” of glyocytes and basic substance of mucopolysaccharide origin are the morphologic basis of hematoencephalic barrier. Hematoencephalic barrier regulates metabolic processes between blood and cerebrospinal fluid. It realizes protective function from the alien agents and products of disorder of metabolism. The most alterations are observed in reticular formation of the middle brain.
In purulent meningitis some pathogenic moments are promoted by rows of paradoxical appearances in hematoencephalic barrier and membranes of the brain. In physiological conditions hematoencephalic barrier and brain’s membranes create closed space, preventing brain’s tissue from influence of environment. In this case secretion and resorbtion of cerebrospinal fluid are proportional. In meningitis closed space leads to increased intracranial pressure due to hypersecretion of cerebrospinal fluid and to edema of the brain. The degree of swelling-edema of the brain is decisive factor in the outcome of the disease.
The next stages may single out in pathogenesis of purulent meningitis:
1. Penetration of the agent through hematoencephalic barrier, irritation of receptors of soft cerebral membrane of the brain and systems, forming cerebrospinal fluid.
2. Hypersecretion of cerebrospinal fluid.
3. Disorder of circulation of the blood in the vessels of the brain and brain’s membranes, delay of resorbtion of cerebrospinal fluid.
4. Swelling-edema of the brain hyperirritation of the brain’s membranes and radices of cerebrospinal nerves.
Besides that, intoxication has essential meaning in pathogenesis of purulent meningitis. Vascular plexuses and ependime of ventricles are damaged more frequently. Then the agent enters in to subarachnoid space and brain’s membranes with the spinal fluid flow.
In some cases, especially in increated patients the process may turn into ependima of the ventricles. As a result it may be occlusion of the foramina of Lushka, Magendie, the aqueduct of Sylvius. It leads to development to hydrocephaly.
In the pathogenesis of meningococcal infection toxic and allergic components play an important role. Thus, in fulminate forms of meningococcal infection infectious-toxic shock develops due to massive destruction of meningococcus and liberaton of considerable quantity of endotoxin. In infectious-toxic shock the development of thrombosis, hemorrhages, necrosis in different organs are observed even in the adrenal glands (Waterhause – Fridrechsen syndrome).
The severe complication may develop as a result of expressive toxicosis. It is cerebral hypertension, leading frequently to lethal outcome, cerebral coma. This state develops due to syndrome of edema swelling of the brains with simultaneous violation of outflow of cerebrospinal fluid and its hyperproduction. The increased volume of the brain leads to pressure of brain’s matter, its removement and wedging of medulla oblongata into large occipital foramen, pressure of oblong brain, paralysis of breath and cessation of cardiovascular activity.
Morbid anatomy
In meningococcal infection pathologoanatomical changes depend on form and duration of the disease.
Nasopharingitis is characterized by hyperemia of the pharyngeal walls, edema of the epithelial cells, regional infiltration, hyperplasion and hyperthophy of lymphoid follicles. Signs of catarrhic inflammation are found in trachea and bronchi.
Cases of fulminate meningococcal infection is characterized by blood vessels disorders and severe impairments of blood circulation. The main target are the microcirculation vessels. The vascular lumen turns narrow, thrombs are found. Thrombs are usually found in small veins. Hemorrhages into skin, subcutaneous tissue, lungs, myocardium, subendocardial hemorrhages, hemorrhages into renal parenchyma, adrenals, brain (Fig.15) and subarachnoidal space are typical.
Fig.15. Hemorrhages into brain
Fig.16. Purulent inflammation
Meningococcous meningitis is characterized by serous or purulent inflammation of pia mater (Fig.16).
Clinical manifestation
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The incubation period is 1-10 days, more frequently 5-7 days.
Classification of the clinical forms of meningococcal infection:
I. Primarily localized forms:
a) meningococcal carrier state
b) acute nasopharyngitis;
c) pneumonia.
II. Gematogenously generalized forms:
a) meningococcemia: typical acute meningococcal sepsis; chronic;
b) meningitis; meningoencephalitis;
c) mixed forms (meningococcemia + meningitis, meningoencephalitis).
d) rare forms (endocarditis, arthritis, iridocyclitis).
In meningococcal carriers the clinical manifestations are absent.
Meningococcal nasopharingitis
The most common complains of the a patients are headache, mainly in the frontal-parietal region, sore throat, dry cough, blocked nose, fatigue, weakness, loss of appetite, violation of the sleep. In most of the patients body temperature rises upto subfebrile and lasts for not more than 3-7 days, sometimes 5-7 days. The skin is pale, conjunctival vessels and sclera are injected. There are hyperemia and edema of the mucous membrane of the nose. In many patients the posterior wall of the pharynx seem to be covered by mucous or mucous – purulent exudation.
Inflammatory changes in the nasopharynx can be noticed after 5-7 days, hyperplasion of lymphoid follicles lasts longer (till 14-16 days). In the peripheral blood temperate leukocytosis with neutrophylosis and a shift of leukocytaric formula to the left, increase in ERS may be revealed. Nasopharyngitis precedes to development of generalized forms of the disease.
Meningitis
It may start after meningococcal nasopharyngitis, but sometimes primary symptoms of the disease arise suddenly. In meningitis three symptoms are revealed constantly: fever, headache and vomiting. Temperature is increases quickly with chill and may reach 40-41°C during few hours. Intermittent, remittent, constant, double waved types of the temperature occur in meningitis. The patients suffer from severe headache, having diffuse or pulsatory character. Headache is very intensive at the night. It increases due to change of body position, sharp sounds, bright light. Vomiting arises without precedent nausea. There is no connection with food and relief after vomiting. It is rule abundant, by “fountain”, repeated. Sometimes, vomiting arises on the peak of headache.
In meningitis hyperthermia, hyperkynesia, photophobia, hyperalgesia, hyperosmia are noticed. These symptoms are revealed more frequently in children. The severe convulsions arise in the many patients at the first hours of the disease (clonic, tonic or mixed types). In small children meningococcal meningitis may start with convulsions.
The disorders of consciousness occupy the great place in clinical picture (from sopor till coma). The loss of consciousness develops after psychomotoric excitement. The loss of consciousness at the first hours of the disease is unfavorable sign.
During objective examination meningeal symptoms stand at the first place. It is described near 30 meningeal signs. A few meningeal signs are used in practice: rigidity of occipital muscles, Kernig’s symptom, Brudzinsky’s symptom (upper, middle and lower). The estimate of state of fontanelle is very important in infants. There are three symptoms of meningitis in infant: swelling, tension and absence of fontanelles pulsation.
There is no accordance between expression of meningeal syndrome and severity of the disease. The expression of different symptoms is no similar at the same patient. The patient has compulsory pose during serious cases. He lays on side with deflection of the head backwards (Fig.17). The legs are curved in knee-joint and pelvic-femoral joint. The legs are pulled to abdomen. Asymmetry and increased tendinous, periostal and dermal reflexes are observed in the patients. These reflexes may be decreased during expressive intoxication. Pathological reflexes may be revealed (such as Babinski’s, Hordon’s, Rossolimo’s reflexes, foot’s clones), and also symptoms of damage cranial nervous (more frequently III, VI, VII, VIII pairs).
Fig.17. Patient’s specific pose in case of meningitis
The multiple symptoms of the lesion of the other organs and systems are connected with intoxication. There is tachycardia at the first hours of the disease. Then it may be bradycardia. Arrhythmia, tachypnoea (30-40 times in minute) are possible. The tongue is covered by dirty brownish coat. It is dry. Abdomen is pulled inside. There is tension of abdomen muscles.
The external appearance of the patients is very typical. There is hyperemia of the face and neck. Sclera’s vessels are injected.
In hemogram high leukocytosis, neuthrophylosis with shift of formula to the left, increased ERS are observed. Small proteinuria, microhematuria, cylinderuria are marked in urine.
Meningococcal meningitis is characterized by acute onset of intense headache, fever, nausea, vomiting, photophobia, and stiff neck. Elderly patients are prone to have an altered mental state and a prolonged course with fever.
Lethargy or drowsiness in patients frequently is reported. Stupor or coma is less common. If coma is present, the prognosis is poor.
Patients also may complain of skin rash, which usually points to disease progression.
The clinical pattern of bacterial meningitis is quite different in young children. Bacterial meningitis in these patients usually presents as a subacute infection that progresses over several days.
Projectile vomiting may occur in children.
Seizures occur in 40% of children with meningitis, typically during the first few days. The majority of seizures have a focal onset.
In infants, the illness may have an insidious onset; stiff neck may be absent. In children, even when the combination of convulsive status epilepticus and fever is present, the classic signs and symptoms of acute bacterial meningitis may not be present.
The Waterhouse-Friderichsen syndrome may develop in 10-20% of children with meningococcal infection. This syndrome is characterized by large petechial hemorrhages in the skin and mucous membranes, fever, septic shock, and DIC.
Neurologic signs of meningococcal meningitis include nuchal rigidity (eg, Kernig sign, Brudzinski sign), lethargy, delirium, coma, and convulsions.
Irritability is a common presenting feature in children.
However, in a 2008 published cohort study from Netherlands (the Meningitis Cohort Study), conducted in adult patients with meningococcal meningitis, only 70% of the patients had the classic triad of fever, neck stiffness, and change in mental status. If the presence of rash was added, 89% of the patients had 2 of the 4 features.
Patients older than 30 years were noted to have petechiae (62%) less frequently than younger patients (81%).
A more severe, but less common form of meningococcal disease, is meningococcal septicemia, which is characterized by rapid circulatory collapse and a hemorrhagic rash.
A petechial or purpuric rash usually is found on the trunk, legs, mucous membranes, and conjunctivae. Occasionally, it is on the palms and soles. The rash may progress to purpura fulminans, when it usually is associated with multiorgan failure (ie, Waterhouse-Friderichsen syndrome). The petechial rash may be difficult to recognize in dark-skinned patients.
Fulminate course of meningitis
With syndrome of brain’s swelling and edema is the most unfavorable variant. There is hypertoxicosis during this form and high percentage of mortality. The main symptoms are consequence of inclination of the brain in to foramen magnum and strangulation of medulla oblongata by tonsils of cerebellum. Immitant symptoms from cardiovascular and respiratory systems develop quickly. Bradycardia appears. Then it is changed by tachycardia. Arterial pressure may fall catastrophically, but it increases more frequently till high level. Tachypnoea arises (till 40-60 times/min) with help of axillary muscles. The disorders of breath lead to its sudden interruption. These symptoms develop in hyperthermia, clonic cramps and loss of consciousness. Cyanosis of the skin, hyperemia of the face are marked. Pyramidal signs, sometimes symptoms of damage of cranial nerves, decreased corneal reflexes contraction of pupils and its decreased reaction on light are determined. Death occurs due to respiratory failure at the first hours of the disease, rarely on 2-3 day or on 5-7 day.
Meningitis with syndrome of cerebral hypotension
It is rare variant of the course of meningococcal meningitis. It is observed principally in children.
The disease develops impetuously, with sharp toxicosis and exicosis. Stupor develops quickly. Cramps are possible. Meningeal signs are no expressive, because, the diagnostics is difficult. Intracranial pressure rapidly falls. In this case the volume of the fluid in the brain’s ventricles decreases. Ventricular collapse develops. In infant the large fontanelle is depressed. In adults and children supporting moments in diagnostics are clinical signs of dehydration and hypotension of cerebrospinal fluid, which flows out by rare drops. The fall of intracranial pressure may lead to development of severe complication – subdural hematoma.
Meningitis with syndrome of ependimatitis (ventriculitis)
Now it is rare form of meningitis. This form develops during late or insufficient treatment of the patients. Especial severity of the disease is connected with spread of inflammation on ventricles membranes (ependime) and involvement of brain’s substance in to pathological process.
The principal clinical symptoms are total and expressive muscular rigidity. The patients accept the particular pose. The disorder of psychic, sleeping, tonic and clonic cramps are observed. The body temperature is normal or subfebrile during general severe state of the patient. Vomiting is constant symptom. Hydrocephalia and cachexia develop due to prolonged course and (or) noneffective therapy of ependimatitis.
Meningoencephalitis
It is rare form of meningococcal infection. In this case the symptoms of encephalitis predominate, but meningeal syndrome is weakly expressed. Meningococcal encephalitis is characterized by rapid onset and impetuous cramps, paresises and paralyses. Prognosis is unfavorable. The mortality is high and recovery is incomplete even in modern conditions.
Meningococcemia (meningococcal sepsis)
The disease is more impetuous, with symptoms of toxicosis and development of secondary metastatic foci. The onset of the disease is an acute. Body temperature may increase upto 39-41 0C and lasts for 2-3 days. It may be continous, intermittent, hectic, wave-like. It is possible the course of the disease without fever. There is no accordance between degree of increasing of the temperature and severity of the course of the disease.
The other symptoms of intoxication arise simultaneously with fever: headache, decreased appetite or its absence, general weakness, pains in the muscles of the back and limbs. Thirst, gryness in the mouth, pale skin or cyanosis, tachycardia and sometimes dysphnoea are marked. The arterial pressure increases in the beginning of the disease. Then it decreases. It may be decreased quantity of urine. Diarrhea may be in some patients. It is more typical for children.
Exanthema is more clear, constant and diagnostically valuable sign of meningococcemia.
Fig.18. Exanthema in case of meningococcemia
Dermal rashes appear through 5-15 hours, sometimes on the second day from the onset of the disease. In meningococcal infection rash may be different over character, size of rash’s elements and localization. Hemorrhagic rash is more typical (petechias, ecchymosis and purpura).
The elements of the rash have incorrect (“star-like”) ( Fig.18) form, dense, coming out over the level of the skin. Hemorrhagic rash is combined inrarely with roseolous and papulous rash.
The severe development of the rash depends from the character, size and depth of the its elements. The deep and extensive hemorrhages may be necrosed. Then it may be formation of deep ulcers. Sometimes deep necrosis is observed on the limbs and also, necrosis of the ear, nose and fingers (Fig.19) of the hands and legs (Fig.20).
Fig.19. Necrosis of fingers
Fig.20. Zones of leg necrosis
During biopsy meningococci are revealed. Exanthema is leucocytaric-fibrinous thrombosis, contained the agent of meningococcal infection. Thus, in meningococcal infection rash is the secondary metastatic foci of the infection.
Joints occupy the second place over localization of metastases of the agent. At the last years arthritises and polyarthritises are marked rarely (in 5 % of the patient during sporadic morbidity and in 8-13 % of the patient during epidemic outbreaks). The small joints are damaged more frequently. Arthritis is accompanied by painful motions, hyperemia and edema of the skin over joints.
Arthritises appear later then rash (the end of the first week – the beginning of the second week of the disease).
Secondary metastatic foci of the infection may appear rarely in the vascular membrane of the eye, in myocardium, endocardium, lungs and pleura. Similar foci arise very rarely in kidneys, liver, urinary tract, borne marrow.
In the peripheral blood high leukocytosis, neuthrophillosis with shift of the formula to the left aneosinophyllia, increased ESR are observed. Thrombocytopenia develops inrarely.
There are alterations in urine as during syndrome of “infectious-toxic kidneys”. Proteinuria, microhematuria, cylinderuria are marked.
Meningococcal sepsis is combined with meningitis in majority cases. In 4-10 % of the patients meningococcemia may be without damage of the soft cerebral covering. Frequency of meningococcal sepsis is usually higher in the period of epidemic.
It is the more severe, unfavorable form of meningococcal infection. Its base is infectious-toxic shock. Fulminate sepsis is characterized by acute sudden beginning and impetuous course. Temperature of body rises up to 40-41 oC. It is accompanied by chill. However, hypothermia may be observed through some hours. Hemorrhagic plentiful rash appears at the first hours of the disease with tendency to confluence and formation large hemorrhages, necroses. A purple-cyanotic spots arise on the skin (“livors mortalis”). The skin is pale, but with a total cyanosis. Patients are anxious and excited. The cramps are observed frequently, especially in children. The recurrent blood vomiting arise inrarely. Also, a bloody diarrhea may be too. Gradually, a prostration becomes more excessive and it results is a loss of the consciousness.
Heat’s activity decreases catastrophically. Anuria develops (shock’s kidney). Hepatolienalic syndrome is revealed frequently. Meningeal syndrome is inconstant.
In the peripheral blood hyperleukocytosis (till 60*109/l), neutrophylosis, sharp shift leukocytaric formula to the left, thrombocytopenia, increased ESR (50-70 mm/h) are reveled. The sharp disorders of hemostasis are marked – metabolic acidosis, coagulopathy of consumption, decrease of fibrinolitic activity of the blood and other.
Mixed forms (meningococcemia + meningitis)
These forms occur in 25-50 % cases of generalized meningococcal infection. In the last years there is tendency of increase frequency of mixed forms in general structure of the disease, especially in periods of epidemic outbreaks. It is characterized by combination of symptoms of meningococcal sepsis and damage of cerebral membranes.
Rare forms of meningococcal infections
These forms (arthritis, polyarthritis, pneumonia, iridocyclitis) are consequence of meningococcemia. Prognosis is favorable in opportune and sufficient therapy.
Diagnostics
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The diagnosis of all forms of meningococcal infection is based on the complex of epidemiological and clinical data. The final diagnosis is established with help of the laboratory examination. Separate methods have different diagnostical significance in various clinical forms of meningococcal infections.
The diagnosis of meningococcal carrier is possible only by use of bacteriological method. The material for analysis is the mucus from proximal portions of upper respiratory tract. In diagnostics of meningococcal nasopharyngitis epidemiological and bacteriological methods occupy the main place. Clinical differention of meningococcal nasopharyngitis from nasopharyngitis of the other genesis is no possible or very difficult.
In recognition of generalized forms, anamnestical and clinical methods of diagnostics have real diagnostic significance, mainly in combination of meningococcemia and meningitis.
The examination of cerebrospinal fluid (CSF) has great meaning in diagnostics of meningitis. In lumbar punction cerebrospinal fluid flows out under high pressure and by frequent drops. The cerebrospinal fluid may flow out by rare drops only due to increased viscosity of purulent exudation or partial blockade of liquor’s ways. Cerebrospinal fluid is opalescent in initial stages of the disease. Then it is turbid, purulent, sometimes with greenish shade (Fig.21).
Fig.21. Cerebrospinal fluid in meningococcal meningitis
Pleocytosis achieves till 10-30 103 in 1 mcl. Neuthrophils leukocytes predominate in cytogram. Neuthrophilous compose 60-100% of all cells. In microscopy neuthrophils cover intirely all fields of vision, inrarely. Quantity of protein of cerebrospinal fluid increases (till 0,66-3,0 g/l). There is positive Nonne-Appelt’s reaction. The reaction of Pandy composed (+++). Concentration of glucose and chlorides are usually decreased.
In generalized forms the final diagnosis is confirmed by bacteriological method. In diagnostics immunological methods are used too. Reactions of hemagglutination, latex agglutination are more sensitive.
CSF Examination
Typical CSF abnormalities in meningitis include the following:
- Increased opening pressure (>180 mm water)
- Pleocytosis of polymorphonuclear leukocytes (white blood cell [WBC] counts between 10 and 10,000 cells/µL, predominantly neutrophils)
- Decreased glucose concentration (< 45 mg/dL)
- Increased protein concentration (>45 mg/dL)
Gram stain and culture of CSF identify the etiologic organism, N meningitides. In bacterial meningitis, Gram stain is positive in 70-90% of untreated cases, and culture results are positive in as many as 80% of cases.
More specialized laboratory tests, which may include culture of CSF and blood specimens, are needed for identification of N meningitidis and the serogroup of meningococci, as well as for determining its susceptibility to antibiotics.
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Differential diagnosis
In meningococcemia the presence of rash requires of differential diagnostics with measles, scarlet fever, rubella, diseases of the blood (thrombocytopenic purpura Werlgoff’s disease; hemorrhagic vasculitis – Sheinlein-Henoch’s disease). Sometimes it is necessary to exclude epidemic typhus, grippe, hemorrhagic fevers.
It is necessary to differentiate meningococcal meningitis with extensive group of the diseases:
1. Infectious and noninfectious diseases with meningeal syndrome but without organic damage of central nervous system (meningismus). Meningismus may be in grippe, acute shigellosis, uremia, lobar pneumonia, toxical food-borne infectious, typhoid fever, epidemic typhus, infectious mononucleosis, pielitis, middle otitis.
2. Diseases with organic damage of central nervous system, but without meningitis (brain abscess, tetanus, subarachnoid hemorrhage).
3. Meningitis of other etiology. In purulent meningitises etiological factors may be pneumococci, staphylococci, streptococci, bacterium coli, salmonella, fungi, Haemophilus influenzae. In purulent meningitis nonmeningococcal etiology it is necessary to reveal primary purulent focus(pneumonia, purulent processes on the skin, otitis, sinusitis, osteomyelitis).
The therapeutic tactics depends from the clinical forms, severity of the course of the disease, presence of complications, premordal state. In serious and middle serious course of nasopharyngitis antibacterial remedies are used. Peroral antibiotics oxacillin, ampyox, chloramphenicol, erythromycin are used.
The duration of the therapy is 3-5 days and more. Sulfonamides of prolonged action are used in usual dosages. In light duration of nasopharyngitis the prescription of antibiotics and sulfonamides is no obligatory.
In therapy of generalized forms of meningococcal infection the central place is occuped by antibiotics, in which salt benzil penicillin stands at the first place. Benzyl penicillin is used in dosage of 200,000-300,000 IU/kg/day. In serious form of meningococcal infection daily dosage may be increased to 500,000 IU/kg/day. Such doses are recommended particularly in meningococcal meningoencephalitis. In presence of ependimatitis or in signs of consolidation of the puss the dose of penicillin increases to 800 000 IU/kg/day.
In similar circumstances it is necessary to inject sodium salt of penicillin by intravenously in dose 2 000 000-12 000 000 units in day. Potassium salt of penicillin is no injected by intravenously, because it is possible the development of hyperkalemia. Intramuscular dose of penicillin is preserved.
Endolumbar injection of penicillin is no used practically last years. Daily dose is injected to the patient every 3 hours. In some cases interval between injections may be increased up to 4 hours. The duration of the therapy by penicillin is decided individually depending on clinical and laboratory data. The duration of penicicllin therapy usually 5-8 days.
At the last years increased resistant strains of meningococcus are marked (till 5-35%). Besides that, in some cases the injection of massive doses of penicillin leads to unfavorable consequences and complications (endotoxic shock, hyperkalemia due to using of potassium salt of penicillin, necroses in the places of injections and other). Also, the patients occur with allergy to penicillin and severe reactions in anamnesis. In such cases it is necessary to perform etiotropic therapy with use other antibiotics. In meningococcal infection semisynthetic penicillins are very effective. These remedies are more dependable and preferable for “start-therapy” of the patients with purulent meningitis till establishment etiological diagnosis. In meningococcal infection ampicillin is the best medicine, which is prescribed in dosage 200-300 mg/kg/day intramuscularly every 4 hours.
In the most serious cases the part of ampicillin is given intravenously. Daily dose is increased to 400 mg/kg/day. Oxacillin is used in dose not less than 300 mg/kg/day every 3 hours. Metycyllin is prescribed in dose – 200-300 mg/kg every 4 hours. In meningococcal infection chloramphenicol is highly effective. It is the medicine of the choice in fulminate meningococcemia. It is shown, that endotoxic reactions arise more rarely during treatment of the patients by chloramphenicol than during therapy by penicillin. In cases of meningoencephalitis chloramphenicol is not prescribed due to its toxic effects on neurons of brain. Chloramphenicol is used in dose 50-100 mg/kg 3-4 ties a day. In fulminate meningococcemia it is given intravenously every 4 hours till stabilization of arterial pressure. Then chloramphenicol is injected intramuscularly. The duration of the treatment of the patients by this antibiotic is 6-10 days.
There are satisfactory results of the treatment of meningococcal infection by remedies from the group of tetracycline. Tetracycline is injected in dose 25 mg/kg intramuscularly and intravenously in the cases of resistant agents to the other antibiotics.
Pathogenetic therapy has exceptional significance in therapeutic measures. It is performed simultaneously with etiotropic therapy. The basis of pathogenetic therapy is the struggle with toxicosis. Salt solutions, macromolecular colloid solutions, plasma, albumin are used. Generally 50-40 ml of fluid is injected on 1 kg of body’s mass per day in adults under the control of diuresis. Prophylaxis of hyperhydratation of the brain is performed simultaneously. Diuretics (lasix, uregit) are injected. In serious cases glucocorticosteroids are prescribed. Full doses is determined individually. It depends on dynamics of the main symptoms and presence of complications. Generally hydrocortisone is used in dose of 3-7 mg/kg/day, prednisolone – 1-2 mg/kg/day. Oxygen therapy has great significance in the treatment of the patients
The therapy of fulminate meningococcemia includs the struggle with shock. Adrenaline and adrenomimetics are not used due to possibility of capillary spasm, increased hypoxia of the brain and kidneys and development of acute renal failure. The early hemodialysis is recommended in the case of acute renal failure due to toxicosis.
The basis of the therapy of infectious-toxic shock is complex of measures, including application of antibiotics, improvement of blood circulation. The course of infectious-toxic shock is very serious, with high mortality (50% of the patient die during the first 48 hours of the disease). Because, it is necessary to prescribe intensive therapy immediately. Antibiotics of wide spectrum of action are prescribed. Steroid hormones have important meaning in the treatment of infectious-toxic shock. Hormones decrease general reaction of the organism on toxin, positively act on hemodynamics. Treatment by glucocorticoids is conducted during 3-4 days.
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Prophylaxis
Prophylactic measures, directional on the sources of meningococcal infection include early revelation of the patients, sanation of meningococcal carriers, isolation and treatment of the patients. Medical observation is established in the focuses of the infection about contact persons during 10 days.
The measures against of the transmissive mechanism, are concluded in performance of sanitary and hygienic measures and disinfection. It is necessary to liquidate the congestion, especially in the closed establishments (children’s establishments, barracks’s and other). The humid cleaning with using of chlorcontaining disinfectants, frequent ventilation, ultra-violet radiation are performed at the lodgings.
The measures, directional on receptive contingents, include increase nonspecific resistance of the people (tempering, timely treatment of the diseases of respiratory tract, tonsils) and formation of specific protection from meningococcal infection. Active immunization is more perspective with help of meningococcal vaccines. There are several vaccines, for example, polysaccharide vaccines A and C.
Vaccine from meningococcus of the group B was also obtained. However, the group B capsular polysaccharide is not sufficiency immunogenic to produce a reliable antibody response in humans to be effective, several solutions to this problem are being studied, including the chemical alterations of the capsular B antigen to make it more immunogenic and the search for other cell wall antigens that are capable of eliciting bactericidal antibodies against B meningococci with a minimum of serious side effects. New vaccines against meningococcus are under development.
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