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Most 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, 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:
- 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 specifically recommended due to its high occurrence, but can be performed to determine their immune status.
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). Sharing of food, eating and drinking utensils, and contact with toddlers' saliva should be avoided.
- 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 woman 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-feeding 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.
Treatment with hyperimmune globulin in mothers with primary CMV infection has been shown to be effective in preventing congenital disease in several studies. One study did not show significant decrease in the risk of congenital cytomegalovirus infection.
Sixty percent of mothers of preterm infants are infected with cytomegalovirus (CMV). Infection is asymptomatic in most instances but 9% to 12% of postnatally infected low birth weight, preterm infants have severe, sepsis-like infection. CMV infection duration can be long and result in pneumonitis in association with fibrosis. CMV infection in infants has an unexpected effect on the white blood cells of the immune system causing them to prematurely age. This leads to a reduced immune response similar to that found in the elderly.
An individual may only develop signs of an infection after a period of subclinical infection, a duration that is called the incubation period. This is the case, for example, for subclinical sexually transmitted diseases such as AIDS and genital warts. Individuals with such subclinical infections, and those that never develop overt illness, creates a reserve of individuals that can transmit an infectious agent to infect other individuals. Because such cases of infections do not come to clinical attention, health statistics can often fail to measure the true prevalence of an infection in a population, and this prevents the accurate modeling of its infectious transmission.
Human immunodeficiency virus type I (HIV) infection can occur during labor and delivery, in utero through mother-to-child transmission or postnatally by way of breastfeeding. Transmission can occur during pregnancy, delivery or breastfeeding. Most transmission occurs during delivery. In women with low detectable levels of the virus, the incidence of transmission is lower. Transmission risk can be reduced by:
- providing antiretroviral therapy during pregnancy and immediately after birth
- delivery by caesarean section
- not breastfeeding
- antiretroviral prophylaxis in infants born to mothers with HIV.
A low number of women whose HIV status are unknown until after the birth, do not benefit from interventions that could help lower the risk of mother-to-child HIV transmission.
Immunodeficiency or immunosuppression can be caused by:
- Malnutrition
- Fatigue
- Recurrent infections
- Immunosuppressing agents for organ transplant recipients
- Advanced HIV infection
- Chemotherapy for cancer
- Genetic predisposition
- Skin damage
- Antibiotic treatment leading to disruption of the physiological microbiome, thus allowing some microorganisms to outcompete others and become pathogenic (e.g. disruption of intestinal flora may lead to "Clostridium difficile" infection
- Medical procedures
- Pregnancy
- Ageing
- Leukopenia (i.e. neutropenia and lymphocytopenia)
The lack of or the disruption of normal vaginal flora allows the proliferation of opportunistic microorganisms and will cause the opportunistic infection - bacterial vaginosis.
Babies can also become infected by their mothers during birth. Some infectious agents may be transmitted to the embryo or fetus in the uterus, while passing through the birth canal, or even shortly after birth. The distinction is important because when transmission is primarily during or after birth, medical intervention can help prevent infections in the infant.
During birth, babies are exposed to maternal blood, body fluids, and to the maternal genital tract without the placental barrier intervening. Because of this, blood-borne microorganisms (hepatitis B, HIV), organisms associated with sexually transmitted disease (e.g., "Neisseria gonorrhoeae" and "Chlamydia trachomatis"), and normal fauna of the genitourinary tract (e.g., "Candida albicans") are among those commonly seen in infection of newborns.
Fever and sickness behavior and other signs of infection are often taken to be due to them. However, they are evolved physiological and behavioral responses of the host to clear itself of the infection. Instead of incurring the costs of deploying these evolved responses to infections, the body opts to tolerate an infection as an alternative to seeking to control or remove the infecting pathogen.
Subclinical infections are important since they allow infections to spread from a reserve of carriers. They also can cause clinical problems unrelated to the direct issue of infection. For example, in the case of urinary tract infections in women, this infection may cause preterm delivery if the person becomes pregnant without proper treatment.
The embryo and fetus have little or no immune function. They depend on the immune function of their mother. Several pathogens can cross the placenta and cause (perinatal) infection. Often, microorganisms that produce minor illness in the mother are very dangerous for the developing embryo or fetus. This can result in spontaneous abortion or major developmental disorders. For many infections, the baby is more at risk at particular stages of pregnancy. Problems related to perinatal infection are not always directly noticeable.
Bats recovering from white-nose syndrome (WNS) may be the first natural occurrence of IRIS, in a report released by the USGS. WNS is typified by a cutaneous infection of the fungus "Pseudogymnoascus destructans" during hibernation, when the immune system is naturally suppressed to conserve energy through the winter. This study suggests that bats undergoing an intense inflammation at the site of infection after a return to euthermia is a form of IRIS.
Since opportunistic infections can cause severe disease, much emphasis is placed on measures to prevent infection. Such a strategy usually includes restoration of the immune system as soon as possible, avoiding exposures to infectious agents, and using antimicrobial medications ("prophylactic medications") directed against specific infections.
Congenital toxoplasmosis is a specific form of toxoplasmosis in which an unborn fetus is infected via the placenta. Congenital toxoplasmosis is associated with fetal death and abortion, and in infants, it is associated with neurologic deficits, neurocognitive deficits, and chorioretinitis. A positive antibody titer indicates previous exposure and immunity, and largely ensures the unborn fetus' safety. A simple blood draw at the first prenatal doctor visit can determine whether or not a woman has had previous exposure and therefore whether or not she is at risk. If a woman receives her first exposure to "T. gondii" while pregnant, the fetus is at particular risk.
Not much evidence exists around the effect of education before pregnancy to prevent congenital toxoplasmosis. However educating parents before the baby is born has been suggested to be effective because it may improve food, personal and pet hygiene. More research is needed to find whether antenatal education can reduce congenital toxoplasmosis.
For pregnant women with negative antibody titers, indicating no previous exposure to "T. gondii", serology testing as frequent as monthly is advisable as treatment during pregnancy for those women exposed to "T. gondii" for the first time dramatically decreases the risk of passing the parasite to the fetus. Since a baby's immune system does not develop fully for the first year of life, and the resilient cysts that form throughout the body are very difficult to eradicate with antiprotozoans, an infection can be very serious in the young.
Despite these risks, pregnant women are not routinely screened for toxoplasmosis in most countries, for reasons of cost-effectiveness and the high number of false positives generated; Portugal, France, Austria, Uruguay, and Italy are notable exceptions, and some regional screening programmes operate in Germany, Switzerland and Belgium. As invasive prenatal testing incurs some risk to the fetus (18.5 pregnancy losses per toxoplasmosis case prevented), postnatal or neonatal screening is preferred. The exceptions are cases where fetal abnormalities are noted, and thus screening can be targeted.
Pregnant women should avoid handling raw meat, drinking raw milk (especially goat milk) and be advised to not eat raw or undercooked meat regardless of type. Because of the obvious relationship between "Toxoplasma" and cats it is also often advised to avoid exposure to cat feces, and refrain from gardening (cat feces are common in garden soil) or at least wear gloves when so engaged. Most cats are not actively shedding oocysts, since they get infected in the first six months of their life, when they shed oocysts for a short period of time (1–2 weeks.) However, these oocysts get buried in the soil, sporulate and remain infectious for periods ranging from several months to more than a year. Numerous studies have shown living in a household with a cat is not a significant risk factor for "T. gondii" infection, though living with several kittens has some significance.
In 2006, a Czech research team discovered women with high levels of toxoplasmosis antibodies were significantly more likely to have baby boys than baby girls. In most populations, the birth rate is around 51% boys, but women infected with "T. gondii" had up to a 72% chance of a boy. In mice, the sex ratio was higher in early latent toxoplasmosis and lower in later latent toxoplasmosis.
IRIS is particularly problematic in cryptococcal meningitis as IRIS is fairly common and can be fatal.
IRIS has been described in immunocompetent hosts who have meningitis caused by "Cryptococcus gattii" and "Cryptococcus neoformans" var. "grubii", environmental fungi which often affect immunocompetent hosts. Several weeks or even months into appropriate treatment, there is a sudden onset deterioration with worsening meningitis symptoms and progression or development of new neurological symptoms.
Magnetic resonance imaging shows increase in the size of brain lesions, and CSF abnormalities (white cell count, protein, glucose) increase. CSF culture is typically sterile, and there is no increase in CSF cryptococcal antigen titer.
The increasing inflammation can cause brain injury or be fatal.
The general mechanism behind IRIS is increased inflammation as the recovering immune system recognizes the antigens of the fungus as immunosuppression is reversed. Cryptococcal IRIS has three phases:
1. before HAART, with a paucity of cerebrospinal fluid (CSF) inflammation and defects in antigen clearance;
2. during initial HAART immune recovery, with pro-inflammatory signaling by antigen-presenting cells without an effector response; and
3. at IRIS, a cytokine storm with a predominant type-1 helper T-cell interferon-gamma response.
Three clinical predictors of cryptococcal-related paradoxical IRIS risk include:
1. lack of initial CSF pleocytosis (i.e. low CSF white blood cell count);
2. elevated C-reactive protein;
3. failure to sterilize the CSF before immune recovery.
IRIS may be the cause of paradoxically worse outcomes for cryptococcal meningitis in immunocompetent compared with immunocompromised hosts, in whom "Cryptococcus neoformans" is the usual pathogen. Treatment with systemic corticosteroids during IRIS may be beneficial in preventing death or progressive neurological deterioration. Steroids given to persons with anti-fungal treatment failure / cryptococcal relapse (in whom CSF cultures are not sterile) can be a fatal iatrogenic error.
When a pregnant woman is diagnosed with acute toxoplasmosis, amniocentesis can be used to determine whether the fetus has been infected or not. When a pregnant woman develops acute toxoplasmosis, the tachyzoites have approximately a 30% chance of entering the placental tissue, and from there entering and infecting the fetus. As gestational age at the time of infection increases, the chance of fetal infection also increases.
If the parasite has not yet reached the fetus, spiramycin can help to prevent placental transmission. If the fetus has been infected, the pregnant woman can be treated with pyrimethamine and sulfadiazine, with folinic acid, after the first trimester. They are treated after the first trimester because pyrimethamine has an antifolate effect, and lack of folic acid can interfere with fetal brain formation and cause thrombocytopaenia. Infection in earlier gestational stages correlates with poorer fetal and neonatal outcomes, particularly when the infection is untreated.
Most household disinfectants will inactivate FHV-1. The virus can survive up to 18 hours in a damp environment, but less in a dry environment and only shortly as an aerosol.
FVR is transmitted through direct contact only. It replicates in the nasal and nasopharyngeal tissues and the tonsils. Viremia (the presence of the virus in the blood) is rare. The virus is shed in saliva and eye and nasal secretions, and can also be spread by fomites. FVR has a two- to five-day incubation period. The virus is shed for one to three weeks postinfection. Latently infected cats (carriers) will shed FHV-1 intermittently for life, with the virus persisting within the trigeminal ganglion. Stress and use of corticosteroids precipitate shedding. Most disinfectants, antiseptics and detergents are effective against the virus.
Cytomegalovirus colitis, also known as CMV colitis, is an inflammation of the colon
Causes
The infection is spread by saliva, urine, respiratory droplets, sexual contact, and blood transfusions. Most people are exposed to the virus in their lifetime, but it usually produces mild or no symptoms in healthy people.
However, serious CMV infections can occur in people with weakened immune systems. This includes patients receiving chemotherapy for cancer and patients on immune-suppressing medicines following an organ transplant.
In rare instances, more severe CMV infection involving the GI tract has been reported in people with a healthy immune system.
As with almost all sexually transmitted infections, women are more susceptible to acquiring genital HSV-2 than men. On an annual basis, without the use of antivirals or condoms, the transmission risk of HSV-2 from infected male to female is about 8–11%.
This is believed to be due to the increased exposure of mucosal tissue to potential infection sites. Transmission risk from infected female to male is around 4–5% annually. Suppressive antiviral therapy reduces these risks by 50%. Antivirals also help prevent the development of symptomatic HSV in infection scenarios, meaning the infected partner will be seropositive but symptom-free by about 50%. Condom use also reduces the transmission risk significantly. Condom use is much more effective at preventing male-to-female transmission than "vice versa". Previous HSV-1 infection may reduce the risk for acquisition of HSV-2 infection among women by a factor of three, although the one study that states this has a small sample size of 14 transmissions out of 214 couples.
However, asymptomatic carriers of the HSV-2 virus are still contagious. In many infections, the first symptom people will have of their own infections is the horizontal transmission to a sexual partner or the vertical transmission of neonatal herpes to a newborn at term. Since most asymptomatic individuals are unaware of their infection, they are considered at high risk for spreading HSV.
In October 2011, the anti-HIV drug tenofovir, when used topically in a microbicidal vaginal gel, was reported to reduce herpes virus sexual transmission by 51%.
Infection in the newborn is accompanied by a strong immune response and is correlated with the need for prolonged mechanical ventilation.
Infection with "U. urealyticum" in pregnancy and birth can be complicated by chorioamnionitis, stillbirth, premature birth, and, in the perinatal period, pneumonia, bronchopulmonary dysplasia and meningitis. "U. urealyticum" has been found to be present in amniotic fluid in women who have had a premature birth with intact fetal membranes.
"U. urealyticum" has been noted as one of the infectious causes of sterile pyuria. It increases the morbidity as a cause of neonatal infections. It is associated with premature birth, preterm rupture of membranes, preterm labor, cesarean section, placental inflammation, congenital pneumonia, bacteremia, meningitis, fetal lung injury and death of infant. "Ureaplasma urealyticum" is associated with miscarriage.
This depends on the age of the animal affected and the efficiency of its immune system.
Colostral protection lasts up to 5 months of age, after which it decreases to an all-time low to increase yet again at about 12 months of age.
- Prenatal infection: virus travels from infected mother to fetus via the placenta. In this case, the time of gestation determines the result of the infection.
- If the fetus is infected in the first 30 days of fetal life, death and absorption of all, or some of the fetuses may occur. In this case, some immunotolerant healthy piglets may be born.
- If the infection happens at 40 days, death and mummification may occur. Also in this case, some or all the fetuses are involved, i.e. some of the fetuses can be born healthy and immunotolerant, or else carriers of the disease.
- If the viruses crosses the placenta in the last trimester, neonatal death may occur, or the birth of healthy piglets with a protective pre-colostral immunity.
- Postnatal infection (pigs up to 1 year of age): Infection occurs oro-nasally, followed by a viremic period associated with transitory leucopenia.
- Infection in adults (over 1 year of age): These subject would have an active, protective immune system which protects them from future exposures (e.g. mating with an infected male).
Therefore, it is important to note that the virus is particularly dangerous for the sow in her first gestation, which would be at 7–8 months of age, as she would have a particularly low antibody count at this age and could easily contract the virus via copulation.
HSV-1 has been proposed as a possible cause of Alzheimer's disease. In the presence of a certain gene variation (APOE-epsilon4 allele carriers), HSV-1 appears to be particularly damaging to the nervous system and increases one's risk of developing Alzheimer's disease. The virus interacts with the components and receptors of lipoproteins, which may lead to its development.
Doxycycline is the drug of choice, but azithromycin is also used as a five-day course rather than a single dose that would be used to treat "Chlamydia" infection; streptomycin is an alternative, but is less popular because it must be injected. Penicillins are ineffective — "U. urealyticum" does not have a cell wall, which is the drug's main target.
Fetal infection is of most consequence as this can result in the birth of a persistently infected neonate. The effects of fetal infection with BVDV are dependent upon the stage of gestation at which the dam suffers acute infection.
BVDV infection of the dam prior to conception, and during the first 18 days of gestation, results in delayed conception and an increased calving to conception interval. Once the embryo is attached, infection from days 29–41 can result in embryonic infection and resultant embryonic death.
Infection of the dam from approximately day 30 of gestation until day 120 can result in immunotolerance and the birth of calves persistently infected with the virus.
BVDV infection between 80 and 150 days of gestation may be teratogenic, with the type of birth defect dependent upon the stage of fetal development at infection. Abortion may occur at any time during gestation. Infection after approximately day 120 can result in the birth of a normal fetus which is BVD antigen-negative and BVD antibody-positive. This occurs because the fetal immune system has developed, by this stage of gestation, and has the ability to recognise and fight off the invading virus, producing anti-BVD antibodies.
Some disease-carrying arthropods use cats as a vector, or carrier. Fleas and ticks can carry pathogenic organisms that infect a person with Lyme disease, tick borne encephalitis, and Rocky mountain spotted fever
BVDV infection has a wide manifestation of clinical signs including fertility issues, milk drop, pyrexia, diarrhoea and fetal infection. Occasionally, a severe acute form of BVD may occur. These outbreaks are characterized by thrombocytopenia with high morbidity and mortality. However, clinical signs are frequently mild and infection insidious, recognised only by BVDV’s immunosuppressive effects perpetuating other circulating infectious diseases (particularly scours and pneumonias).