Every baby is different and has very 1..... needs. Your 2..... baby may need more than twenty hours of sleep a day or she may only 3..... twelve. You’ll find that your baby’s sleep 4..... is as individual as her fingerprint. We give you some information and practical hints to help you 5..... a sound sleep routine with your child.
After nine months of secure, warm comfort, your baby emerges into a strange world of daylight and darkness. For the first few months she’ll 6..... to make any distinction between the two and will 7..... and 8..... whenever it seems right to do so!
At the outset sleep is closely related to 9..... and most babies wake when they are 10..... . You’ll soon begin to recognize her own timetable and rhythms, which will 11..... when she wakes and for how long she remains 12..... at any one time.
As she grows 13..... she will need 14..... sleep as she becomes more and more interested in her surroundings. So by the time she’s about four months old, she 15..... to be wide awake for two or three periods each day. By establishing a pattern for her and by associating night with sleep you will help your baby to settle into a routine pattern of 16..... sleeping.
Your child may wake at night for a variety of 1..... . She may be hungry or thirsty, too 2..... or uncomfortably hot. She may just want a reassuring cuddle or she may be telling you that she is 3..... . She may wake 4..... because she’s poorly or teething. Most of these simply need practical 5..... or are situations that will resolve themselves in time.
Some children seem 6..... for no apparent reason. She may have had a vivid dream or have heard an 7..... noise outside. If she 8....., go to her and pacify her, but try not to bring her out of her room. Check that her room is cosy and quiet and 9..... that the curtains are thick enough to keep out the light. You may 10..... to keep a night light on.
Look at what has happened during the day. Is she getting 11..... enough or is she getting 12..... tired during the day? Can you 13..... anything which may be upsetting or frightening her? Try to avoid wild rough and tumbles just before bed too.
You could 14..... reading to her, rocking her to sleep, singing or playing gentle music. While it may be temping 15..... her into bed with you this habit can be very hard to break so it’s usually 16..... to leave her in her cot and let her settle there.
1. at night; 2. unusual; 3. need; 4. better; 5. identify; 6. to take; 7. reasons; 8. action; 9. to wake; 10. cold; 11. tired; 12. wet; 13. make sure; 14. cries; 15. try; 16. too.
Blood is a fluid which 1..... though the arteries, capillaries and veins exchanging fluids and gases with the bodily 2..... . The latter receive the products 3..... from the food and oxygen taken up by the blood in its passage through the lungs, while the blood 4..... from the tissues carbonic acid gas and various waste products.
Composition. The blood 5..... of corpuscles in addition to the fluid is well-known. They are of the three 6..... : red corpuscles (erythrocytes), white corpuscles (leucocytes) and blood platelets (thrombocytes). In the fluid are dissolved the various salts and 7..... . We know the red corpuscles acting as the 8..... of oxygen, which acts as a medium of interchange between the 9..... of the air in the lungs, and the tissues requiring it. There are over 5000000 red corpuscles in every cubic millimeter of 10..... .
The white corpuscles are of 11..... different kinds, they have many functions to perform, of which the chief are repair of 12..... , the absorption of foreign bodies, and the 13..... of bacteria; their 14..... bodies being in large numbers form the matter or pus of abscesses.
Blood groups. People are 15..... , in respect of certain reaction of the blood, into four groups. Their being divided into these groups 16..... upon the capacity of the serum of one person’s blood to 17..... the red blood corpuscles of another’s. The reaction depends on antigens in the red corpuscles and 18..... in the serum. There are two of each, the antigens being known as A and B. Anyone’s blood 19..... may have (I) no antigens, (II) antigen A, (III) antigen B. (IV) antigens A and B: these are the four groups. The practical 20..... is that, in blood transfusion, the person giving and the person 21..... the blood should belong to the same blood group, or a 22..... reaction will take place from the agglutination.
Many infections such as gastroenteritis 1..... E coli, hepatitis A, typhoid and cholera are water-borne and can 2..... a holiday into a nightmare. Travellers 3..... be advised to give careful attention to personal 4..... , sterilization of drinking 5..... and to the hygiene with which food has been prepared. Breast feeding 6..... a safe, uncontaminated supply of food and water for 7..... and can usually be continued even if the mother 8..... an infection. For 9..... babies, supplies of a ready-to-feed pre-packed formula are ideal. Scrupulous 10..... must always be paid to sterilization of bottle feeds and equipment. Water should be 11..... , as should milk if not pre-packed. Sterilizing water with chlorine tablets is an 12..... method.
Hand 13..... before and after using toilet or changing nappies, sanitary wear or stoma bags is a sensible 14..... . If water is not 15..... , a supply of disposable moist antiseptic cloths is 16..... . Make sure that disposable items are safely wrapped before disposal.
Although we know that AIDS is caused by Human Immunodeficiency Virus (HIV), it was originally observed by its effects on the immune system. An important clue was that AIDS patients often had a lung infection or pneumonia caused by a member of the fungi family of organisms called Pneumocystis carinii. This infection is very rare in healthy individuals but patients with cancers of the immune system itself (lymphomas) are susceptible to this disease. Lymphomas are usually treated by chemotherapy, which is intended to destroy the cancer cells. However, chemotherapy, which is intended to destroy many healthy immune cells along with the cancerous lymphoma cells. Thus, this type of pneumonia predominantly occurs in patients with a damaged immune system. Examination of the immune system in AIDS patients confirmed that the cells of their immune systems were damaged. It had been known for some time that other various virus infections could damage as seen with AIDS was unprecedented. Although it was suspected early on that AIDS resulted from infection by a virus, it was not until 1984 that this virus was finally isolated by both French and American researchers. That virus is now known as HIV.
In addition to pneumonia, AIDS is associated with numerous other infections. These secondary infections are caused by various bacteria, protozoa, other fungi and other viruses. Usually, it is these infections (known as opportunistic infections) that cause death in AIDS patients. In addition to secondary infections AIDS patients frequently develop cancers, including lymphomas and an otherwise rare cancer called Kaposi’s sarcoma. HIV infection also can result in damage to brain cells. This leads to loss of mental function, referred to as AIDS dementia. A more complete description of the clinical features of AIDS is presented further. Most of these opportunistic infections and some other effects of HIV infection can be explained by damage to the immune system by HIV infection.
HIV has a very insidious nature in causing a disease. The early stages of infection are often unapparent, without any visible symptoms. The infected person may feel healthy and appear to be completely normal during this time, known as the incubation period, but such a person is able to transmit the infection. The HIV incubation period is of variable duration, and can be quite long (more than 5 years). Therefore, it is not possible to distinguish infected from uninfected people solely by the time since possible exposure to the virus. In contrast, for most common virus infections, such as colds or influenza, an incubation period of several days will be closely followed by an apparent disease. This adds greatly to the difficulty in studying and controlling AIDS because many people who have the virus have not developed the disease yet.
THE AIDS EPIDEMIC. Despite the many different clinical symptoms associated with AIDS, medical investigations have already learned a great deal about how AIDS is spread in our population. For example, it is now clear that HIV transmission requires close contact and that infection occurs by one of only three routes; blood, birth, or sex. Casual contact does not lead to disease transmission. AIDS epidemiology will be further discussed..
Between 1981 (the beginning of AIDS epidemic) and the early part of 1988 about 57,000 cases of AIDS have been reported to the National Center for Disease Control (CDC) in Atlanta, Georgia. Of these cases, about 32,000 (56%) have died.
Promiscuous homosexual males were the major afflicted group and represent about 63% of these reported cases. Another 18% of the cases were intravenous drug users, and 7% were both male homosexuals transmissions, or by blood transfusion during the period when American blood supply was not monitored for HIV antibodies (1981-1985).
The AIDS epidemic is not restricted to the USA. It can be found in all continents and hence is considered a pandemic. There may be as many as ten million people in sub-Saharan Africa who are infected with HIV. In Africa, HIV transmission appears to result from heterosexual contact and other modes as well. Given the relatively poor medical support available in much of Africa, the number of infected people is expected to increase significantly. As there is no current cure for AIDS these numbers are alarming. They indicate the clear potential of AIDS to spread unchecked, in spite of recent advances in modern medicine, epidemiology, virology, and recombinant DNA technology. This reminds us of previous eras when major infectious diseases devastated human populations. How can we control this epidemic? An overview of the relationship between epidemics and human populations may shed some light on this.
THE EPIDEMIOLOGY OF AIDS IN THE U.S.
Today AIDS has become a major cause of morbidity and mortality in the U.S. Indeed, it has become the leading cause of death in the country among people with hemophilia and users of illegal intravenous (IV) drugs. Moreover, nation-wide morbidity and mortality rates will increase in the next few years as some of the one to 1.5 million Americans who are already infected with the human immunodeficiency virus (HIV) develop AIDS. Most of those drug abusers, and a significant proportion of them will be blacks and Hispanics. Yet, given the fact that the virus is transmitted through sexual contact, through the traces of blood in needles and other drug paraphernalia and from mother to newborn infant, one can envision many possible chains of infection, which leave no segment of the U.S. population completely unaffected by the threat of AIDS.
The discovery of the epidemic, the enumeration of the varied manifestations of HIV infection and the analysis of the circumstances that made it possible for such an infection to spread have been missions assigned to epidemiology: the study of the occurrence and distribution of disease as well as its control in a given population. Epidemiologists monitor mortality and morbidity rates associated with HIV infection and AIDS; they also make predictions of likely changes in HIV infection rates in the course of time.
Most important, by carrying out studies to define the ways HIV is transmitted from person to person, epidemiologists can identify the population groups that are at greatest risk of acquiring AIDS and thereby develop strategies for the prevention and control of the disease – strategies that are independent of the development of an effective vaccine or therapy. Indeed, determining the risk factors for AIDS enabled the U.S. Public Health Service and other groups to issue recommendations for the prevention of AIDS as early as 1983, a full year before HIV was firmly identified and two years before laboratory tests to detect the presence of the virus became widely available.
To carry out all these tasks epidemiologists depend on surveillance: the gathering of high-quality, consistent and interpretable data on a disease or an infection. Surveillance data are routinely compiled from reports filed with state and local health departments that are then forwarded to the U.S. Centers for Disease Control (CDC).
Because the disease appeared to be transmitted through the exchange of blood or by sexual contact, most investigators were convinced by late 1982 that the cause of AIDS was an infectious agent (most likely a virus) and not the result of exposure to toxic substances or other environmental or genetic factors. The infection hypothesis was finally confirmed when HIV was isolated by Luc Montagnier and his colleagues at the Pasteur Institute in Paris and by Robert C. Gallo and his colleagues at the National Cancer Institute.
Soon after the discovery of the AIDS agent a laboratory test was developed to detect antibodies to HIV in the blood. A positive result in a test of a person’s blood sample was a reliable sign that the person was infected with the virus. Such a serological test made it possible to detect HIV infection in people who showed no clinical symptoms, and to confirm clinical diagnoses of AIDS and other HIV-related conditions. It also made it possible to measure directly the prevalence of HIV infection (the number of infected people in a given time) and its incidence (the number of new infections occurring within a defined period in a specific population). Most important, perhaps, was the fact that the national supply of donated blood could now be screened, so that additional cases of AIDS due to blood transfusions and contaminated blood products could be avoided.
RISK OF HIV INFECTION
The possibility that one can become infected with HIV if contaminated blood penetrates the skin or mucous membranes also represents a small but definite occupational risk for health-care workers. In a national collaborative study done by the CDC, four of 870 health-care workers who had accidentally punctured their skin with needles contaminated with the blood of HIV-infected people developed HIV infection, but none of the 104 workers whose mucous membranes or skin had been exposed to blood became infected. In another study of health-care workers at the National Institute of Health, no HIV infections occurred among 103 workers with needle-stick injuries, nor were there any HIV infections among 691 workers who had a total of more than 2000 reported skin and mucous-membrane exposures to blood or body fluids of AIDS patients. The studies are consistent with other data indicating that the occupational risk of acquiring HIV infection in health-care settings is low and is most often associated with percutaneous inoculation of blood from an infected patient.
HIV is also transmitted from an infected mother to her newborn child, but the extent of transmission that takes place respectively during pregnancy, at birth or soon afterward is as yet unknown. Detection of HIV in fetal tissues supports the hypothesis that infection occurs in utero, and case reports of women who became infected with HIV immediately after giving birth, and subsequently infected their infants, suggest that the virus may be transmitted through breast-feeding.
Studies of such perinatal transmission are greatly complicated by the lack of a reliable diagnostic test to determine HIV infection in newborns. As is the case with other infections, infants born to HIV-infected mothers have maternally derived HIV antibodies circulating in their blood – regardless of whether or not they have been infected. The maternal HIV antibodies may persist for as long as 12 months and cannot be distinguished from antibodies that may be present in an infant infected with HIV. Other tests are under development for identifying HIV infection in these newborns. Currently all infants born to infected mothers must be followed closely for at least 12 months to see whether there is any clinical or laboratory evidence of HIV infection or AIDS.
To evaluate the risk of HIV transmission through other casual contacts, several prospective studies (which are carried out over several years) have been done of the families of infected adults and children. In spite of tens of thousands of days of household contact with infected individuals, not one of more than 400 family members has been infected with HIV – except for sexual partners of the infected person and children born to infected mothers. In these studies the documented risk of household transmission was zero, and therefore the actual risk must be extremely low, even in crowded households. The risk of transmission in other social settings, such as schools and offices, is presumably even lower than in household settings.
Epidemiological studies in the U.S. and other countries throughout the world show no patterns of HIV infection consistent with transmission by insect vectors. If HIV were transmitted by insect vectors, additional cases of infection would be seen in people who share environments with infected individuals. Such evidence is lacking, in spite of extensive surveillance efforts.
Although HIV can survive for from several hours to several days in insects artificially fed blood with high concentrations of the virus, there is no evidence that HIV actually grows in insects. Such a biological event is important in most viral diseases transmitted by insects.
To be sure, the existence of other unrecognized modes of HIV transmission can never be entirely excluded, but if they do exist, they appear to be extremely rare.
HIV INFECTION: THE CLINICAL PICTURE
As physicians we are often asked to describe the typical course of AIDS: the severe immune deficiency that enables normally benign organisms to flourish destructively in patients. Our answer is that people are asking the wrong question. Now that AIDS is known to be caused by a virus – the human immunodeficiency virus, or HIV – the focus should be on the full course of the viral infection, not solely on AIDS. HIV causes a predictable, progressive derangement of immune function, and AIDS is just one, late manifestation of that process.
An emphasis on HIV is important because it facilitates both treatment and prevention. Prompt diagnosis of HIV infection enables the patient to receive optimal medical care from the earliest moments of the disease. Such care can often prevent complications from developing or getting unnecessarily out of hand. For instance, the lethal opportunistic infection “Pneumocystis carinii” pneumonia (PCP), which has been a hallmark of AIDS, can now actually be prevented with medication given early in the course of HIV disease. (Opportunistic infections are ones that occur because the immune system has broken down.) In addition, the medicine Retrovir (also known as AZT), which has been shown to prolong life in patients with late-stage disease, holds promise as a therapy for patients in earlier stages of infection. Early diagnosis also eliminates the unwitting transmission of HIV and gives people the opportunity to consider changing their behavior before they pass the virus to others.
Although the continuing emphasis on AIDS alone is seriously misguided, it is somewhat understandable. When AIDS was first identified in 1981, it was a mysterious syndrome: a cluster of rare diseases that had suddenly become alarmingly common in homosexual men. In order to identify similar cases of AIDS, and thereby help to uncover the cause and means of transmission, the U.S.Center for Disease Control (CDC) adopted a strict epidemiological-surveillance definition. People were said to have AIDS if they contracted Kaposi’s sarcoma (a rare cancer) or if they developed any of a few rare opportunistic infections, most notably PCP.
Because we and our colleagues at the Walter Reed Army Medical Center believe HIV-infected patients must be treated on the basis of the fullest possible understanding of their disease, we developed a classification system that provides a framework for managing patients and understanding the progression of the disease. The system groups patients according to their stage of infection.
The Walter Reed classification system begins with stage zero: exposure to the virus through any of the known transmission routes. Noting exposure facilitates early diagnosis: people who are known to have been exposed to HIV can be evaluated for evidence of infection, such as the presence of antibodies to HIV in the blood. Even before infection is detected they can be told that they may be infected with HIV and so should take steps to avoid spreading the possible infection to others; HIV usually causes no symptoms at first can take root from six weeks to a year before it is detected by the standard (antibody) HIV test.
Once the presence of HIV has been documented by any reliable test, patients are said to be in Walter Reed stage 1, provided they do not meet the criteria for a higher stage.
Although most people have no symptoms when HIV infection is first diagnosed, some patients develop a disorder resembling mononucleosis. Its symptoms include fatigue, fever and swollen glands, which may or may not be accompanied by a rash. In addition self-limited disorders of the central nervous system have been noted. These range from headaches to encephalitis (inflammation of brain tissue). The cause of these symptoms is not entirely clear. In any event, they disappear, usually within a few weeks.
For the majority of patients the first sign that something is amiss in the immune system is the development of chronically swollen lymph nodes. With the appearance of this chronic lymphadenopathy a patient moves into stage 2.
Stage 2 typically lasts for from three to five years, and patients still feel well even when it ends. The beginning of stage 3 is defined by a persistent drop in the T4-cell count to less than 400, which is a harbinger of a decline in immune functioning. Patients remain in this stage, however, until direct evidence of an impairment in cell-mediated immunity is discovered – usually about 18 months later – at which point they enter stage 4. That evidence is the failure to respond to three out four skin tests that measure what is called delayed hypersensitivity: the individual’s ability to mount a cellular immune response against specific proteins injected under the skin.
Progression to stage 5 is usually determined on the basis of the development of anergy (a total absence of delayed hypersensitivity). Some time later the first overt symptom of a breakdown in cell-mediated immunity arises: the development of thrush, a fungal infection of the mucous membranes of the tongue or the oral cavity. Thrush is identified by the presence of white spots and ulcers covering the infected area.
In addition to thrush, stage 5 patients often develop unusually severe or persistent viral or fungal infections of the skin and mucous membranes. One example is chronic infection with the Herpes simplex virus, which often produces painful and persistent sores in the skin surrounding the anus, the genital area or the mouth.
Many people develop chronic or disseminated opportunistic infections at sites beyond the skin and mucous membranes within a year or two after entering stage 5. The emergence of these infections reflects an extremely severe decline in immune function and constitutes progression to stage 6, or what is also called opportunistic-infection-defined AIDS. Most patients enter stage 6 with a T4-cell count of 100 or less and most, unfortunately, die within two years.
Any pathogen that can be eradicated only with the help of vigorous cell-mediated immunity can cause serious disease.
In addition to PCP (Pneumocystis carini pneumonia), other disorders associated with AIDS include the parasitic infectious toxoplasmosis (which typically attacks the intestinal tract, causing chronic diarrhea).
Stage 6 opportunistic diseases also include the fungal infectious cryptococeosis (which frequently causes meningitis but may also damage the liver, bone, skin and other tissues), and histoplasmosis (which can cause self-limited pneumonia in individuals with an intact immune system but causes a disseminated infection of the liver, bone marrow and other tissues in HIV-infected patients and is a frequent cause of chronic fevers).
A common viral infection is cytomegalovirus, a cause of pneumonia, encephalitis, blindness and inflammation of the gastrointestinal tract. As is the case with histoplasmosis and tuberculosis, the cytomegalovirus infection seen in HIV patients is usually a reactivation of a childhood infection that was well controlled until HIV seriously hobbled the patient’s immune system. Such bacteria as “Legionella” and “Salmonella” can also be a severe problem for someone in stage 6.
Standard or experimental therapies exist for all these disorders. Among the most exciting developments in recent years is the discovery of several medications that control or even prevent PCP. Pentamidine, Septra/Bactrium and Dapsone are all effective in clearing up the infection; the first two – and a drug called Fansidar – serve as preventives as well.
Also exciting are new treatments for cytomegalovirus. Just two years ago investigators had little hope of discovering an effective therapy for the virus. Today there are two treatments, including a medicine (ganciclovir) that can halt the progression of cytomegalovirus- induced blindness. Research workers are making progress against other HIV-related diseases as well. A drug called acyclovir is under study for the prevention of Herpes simplex infection, and new treatments have been developed for cryptococcal meningitis, disseminated histoplasmosis and mycobacterial diseases.
STRANGE TRIP BACK TO THE FUTURE
Officially, the AIDS epidemic began in the U.S. in 1981. Recently, however, researchers jolted the medical community with evidence that the disease may have made its first appearance in the U.S. almost 15 years earlier. In a front-page article in the Chicago “Tribune”, they related the extraordinary saga of Robert R., a 16-year-old black Missourian who, they believe, died of AIDS in 1969. The case may represent the earliest documented instance of AIDS in North America. Predating that of Gaetan Dugas, a Canadian flight attendant. Dugas, who contracted AIDS before 1980 and died in 1984, was publicly identified as “Patient Zero” only quite recently. Tissue samples from Robert R. may eventually reveal what caused the virus to spread.
Two researchers, microbiologist Memory Elwin-Lewis of Washington University in St. Louis and Marlys Witte, a professor of surgery at the University of Arizona in Tucson, told of a black teenager who showed up at St. Louis City Hospital in 1968 with chronic genital swelling. The youngster, then 15, admitted that he was sexually active; laboratory tests disclosed that he has a severe case of chlamydia, a common but curable venereal disease. Doctors prescribed several antibioyics and put him on a low-salt diet. Nothing worked. His muscles wasted away, and his lungs filled with fluid.Robert R. died on May 15, 1969. An autopsy revealed the distinctive purplish lesions of AIDS-related Kaposi’s sarcoma.
Hoping at the time that medical advances might someday solve the mystery of his affliction, Elwin-Lewis and Witte, then both at Washington University, froze samples of Robert R.’s blood, brain, and other organs. In June 1987, four years after the AIDS virus was first isolated, Witte sent some of the frozen samples to Tulane University, where they were definitely analyzed by Virologist Robert Garry. “There’s no question that the tissue was positive for AIDS”, Garry states. In fact, Robert R.’s blood reacted to all nine markers used in the highly sensitive Western blot test for AIDS antibodies. Why didn’t the researchers have the samples tested earlier? “We waited until the chance of documenting the infection was more likely.” Witte explains.
Robert R.’s case is even more intriguing because he never visited New York City, San Francisco and Los Angeles, the current AIDS epicenters. In fact, he told his doctors, he never left the Midwest. That is not surprising, says Dr. James Curran, director of the AIDS program at the Center for Disease Control. “It’s just not logical that AIDS entered the country only once,” he says. I think that there were several entry points but that most of them occurred in the late 1970s.”
Other presumptive cases are emerging from the past. In New York City in 1959, for example, a 49-year-old Haitian-born shipping clerk fell victim to what today would be a telltale disorder:
“Pneumocystis carinii” pneumonia. “It was so unusual at the time”, recalls Dr. Gordon Hennigar, who performed the postmortem and now is chairman of pathology at the Medical University of South Carolina. “AIDS is such a strong possibility that I’ve often thought about getting the samples and testing them.”
Indeed, the history of AIDS in the U.S. may have a much longer prologue than was once suspected. “What we’re saying is that AIDS has been around for a long time but just wasn’t recognized”, Elwin-Lewis explains. It is possible, Tulane’s Garry speculated, that the AIDS virus mutated and became more lethal in the 1970s. To test that hypothesis, he plans to spend much of the next year or so attempting to reconstruct viral genes from Robert R.’s tissue. “We know that the virus was not epidemic in 1969, so we might be able to identify the changes between then and now that enabled it to spread, Garry says. If scientists can figure out how the AIDS virus might have changed, the puzzling case from the past might shed light on the future of the epidemic.