Dehydration

Definition

Dehydration occurs when you lose more fluid than you take in, and your body doesn't have enough water and other fluids to carry out its normal functions. If you don't replace lost fluids, you may get dehydrated.
Common causes of dehydration include intense diarrhea, vomiting, fever or excessive sweating. Not drinking enough water during hot weather or exercise also may cause dehydration. Anyone may become dehydrated, but young children, older adults and people with chronic illnesses are most at risk.
You can usually reverse mild to moderate dehydration by drinking more fluids, but severe dehydration needs immediate medical treatment. The safest approach is prevention of dehydration. Monitor your fluid loss during hot weather, illness or exercise, and drink enough liquids to replace what you lose.

Symptoms

Mild to moderate dehydration is likely to cause:

• Dry, sticky mouth
• Sleepiness or tiredness — children are likely to be less active than usual
• Thirst
• Decreased urine output — no wet diapers for three hours for infants and eight hours or more without urination for older children and teens
• Few or no tears when crying
• Dry skin
• Headache
• Constipation
• Dizziness or lightheadedness

Severe dehydration, a medical emergency, can cause:

• Extreme thirst
• Extreme fussiness or sleepiness in infants and children; irritability and confusion in adults
• Very dry mouth, skin and mucous membranes
• Lack of sweating
• Little or no urination — any urine that is produced will be dark yellow or amber
• Sunken eyes
• Shriveled and dry skin that lacks elasticity and doesn't "bounce back" when pinched into a fold
• In infants, sunken fontanels — the soft spots on the top of a baby's head
• Low blood pressure
• Rapid heartbeat
• Rapid breathing
• No tears when crying
• Fever
• In the most serious cases, delirium or unconsciousness

Unfortunately, thirst isn't always a reliable gauge of the body's need for water, especially in children and older adults. A better indicator is the color of your urine: Clear or light-colored urine means you're well hydrated, whereas a dark yellow or amber color usually signals dehydration.
When to see a doctor
If you're a healthy adult, you can usually treat mild to moderate dehydration by drinking more fluids, such as water or a sports drink (Gatorade, Powerade, others).
Get immediate medical care if you develop severe signs and symptoms such as extreme thirst, a lack of urination, shriveled skin, dizziness and confusion.
Treat children and older adults with greater caution. Call your family doctor right away if your loved one:

• Develops severe diarrhea, with or without vomiting or fever
• Has bloody stool
• Has had moderate diarrhea for three days or more
• Can't keep down fluids
• Is irritable or disoriented and much sleepier or less active than usual
• Has any of the signs or symptoms of mild or moderate dehydration

Go to the nearest hospital emergency room or call 911 or your emergency medical number if you think a child or older adult is severely dehydrated. You can help prevent dehydration from becoming severe by carefully monitoring someone who is sick and giving fluids, such as an oral rehydration solution (Pedialyte, others) at the first sign of diarrhea, vomiting or fever and by encouraging children to drink plenty of water before, during and after exercise.

Causes

Dehydration occurs when there isn't enough water to replace what's lost throughout the day. Your system literally dries out. Sometimes dehydration occurs for simple reasons: You don't drink enough because you're sick or busy, or because you lack access to safe drinking water when you're traveling, hiking or camping.
Other dehydration causes include:

• Diarrhea, vomiting. Severe, acute diarrhea — that is, diarrhea that comes on suddenly and violently — can cause a tremendous loss of water and electrolytes in a short amount of time. If you have vomiting along with diarrhea, you lose even more fluids and minerals. Children and infants are especially at risk.
• Fever. In general, the higher your fever, the more dehydrated you may become. If you have a fever in addition to diarrhea and vomiting, you lose even more fluids.
• Excessive sweating. You lose water when you sweat. If you do vigorous activity and don't replace fluids as you go along, you can become dehydrated. Hot, humid weather increases the amount you sweat and the amount of fluid you lose. But you can also become dehydrated in winter if you don't replace lost fluids. Preteens and teens who participate in sports may be especially susceptible, both because of their body weight, which is generally lower than that of adults, and because they may not be experienced enough to know the warning signs of dehydration.
• Increased urination. This is most often the result of undiagnosed or uncontrolled diabetes mellitus, a disease that affects the way your body uses blood sugar. This type of diabetes often causes increased thirst and more frequent urination. Another type of diabetes, diabetes insipidus, also is characterized by excessive thirst and urination, but in this case the cause is a hormonal disorder that makes your kidneys unable to conserve water. Certain medications — diuretics, antihistamines, blood pressure medications and some psychiatric drugs — as well as alcohol also can lead to dehydration, generally because they cause you to urinate or perspire more than normal.

Risk factors

Anyone can become dehydrated if they lose too many fluids. But certain people are at greater risk, including:

• Infants and children. Infants and children are especially vulnerable because of their relatively small body weights and high turnover of water and electrolytes. They're also the group most likely to experience diarrhea.
• Older adults. As you age, you become more susceptible to dehydration for several reasons: Your body's ability to conserve water is reduced, your thirst sense becomes less acute and you're less able to respond to changes in temperature. What's more, older adults, especially people in nursing homes or living alone, tend to eat less than younger people do and sometimes may forget to eat or drink altogether. Disability or neglect also may prevent them from being well nourished. These problems are compounded by chronic illnesses such as diabetes, by hormonal changes associated with menopause and by the use of certain medications.
• People with chronic illnesses. Having uncontrolled or untreated diabetes puts you at high risk of dehydration. But other chronic illnesses also make you more likely to become dehydrated. These include kidney disease, alcoholism and adrenal gland disorders. Even having a cold or sore throat makes you more susceptible to dehydration because you're less likely to feel like eating or drinking when you're sick. A fever increases dehydration even more.
• Endurance athletes. Anyone who exercises can become dehydrated, especially in hot, humid conditions or at high altitudes. But athletes who train for and participate in ultramarathons, triathlons, mountain climbing expeditions and cycling tournaments are at particularly high risk. That's because the longer you exercise, the more difficult it is to stay hydrated. During exercise, your body may lose more water than it can absorb. With every hour you exercise, your fluid debt increases. Dehydration is also cumulative over a period of days, which means you can become dehydrated with even a moderate exercise routine if you don't drink enough to replace what you lose on a daily basis.
• People living at high altitudes. Living, working and exercising at high altitudes (generally defined as above 8,200 feet, or about 2,500 meters) can cause a number of health problems. One is dehydration, which commonly occurs when your body tries to adjust to high elevations through increased urination and more rapid breathing — the faster you breathe to maintain adequate oxygen levels in your blood, the more water vapor you exhale.
• People working or exercising outside in hot, humid weather. When it's hot and humid, your risk of dehydration and heat illness increases. That's because when the air is humid, sweat can't evaporate and cool you as quickly as it normally does, and this can lead to an increased body temperature and the need for more fluids.

Complications

Dehydration can lead to serious complications, including:

• Heat injury. If you don't drink enough fluids when you're exercising vigorously and perspiring heavily, you may end up with a heat injury, ranging in severity from mild heat cramps to heat exhaustion to potentially life-threatening heatstroke.
• Swelling of the brain (cerebral edema). Sometimes, when you're getting fluids again after being dehydrated, the body tries to pull too much water back into your cells. This can cause some cells to swell and rupture. The consequences are especially grave when brain cells are affected.
• Seizures. Electrolytes — such as potassium and sodium — help carry electrical signals from cell to cell. If your electrolytes are out of balance, the normal electrical messages can become mixed up, which can lead to involuntary muscle contractions and sometimes to a loss of consciousness.
• Low blood volume shock (hypovolemic shock). This is one of the most serious, and sometimes life-threatening, complications of dehydration. It occurs when low blood volume causes a drop in blood pressure and a drop in the amount of oxygen in your body.
• Kidney failure. This potentially life-threatening problem occurs when your kidneys are no longer able to remove excess fluids and waste from your blood.
• Coma and death. When not treated promptly and appropriately, severe dehydration can be fatal.

Tests and diagnosis

Your doctor can often diagnose dehydration on the basis of physical signs and signs and symptoms such as little or no urination, sunken eyes, and skin that lacks its normal elasticity and resilience when pinched. If you're dehydrated, you're also likely to have low blood pressure, especially when moving from a lying to a standing position, a faster than normal heart rate and reduced blood flow to your extremities.
To help confirm the diagnosis and pinpoint the degree of dehydration, you may have other tests, such as:

• Blood tests. Blood samples may be used to check for a number of factors, such as the levels of your electrolytes — especially sodium and potassium — and how well your kidneys are working.
• Urinalysis. Tests done on your urine can help show whether you're dehydrated and to what degree.

If it's not obvious why you're dehydrated, your doctor may order additional tests to check for diabetes and for liver or kidney problems.

Malaria

Malaria is an infectious disease caused by a parasite, Plasmodium, which infects red blood cells. Malaria is characterized by cycles of chills, fever, pain, and sweating. Historical records suggest malaria has infected humans since the beginning of mankind. The name "mal aria" (meaning "bad air" in Italian) was first used in English in 1740 by H. Walpole when describing the disease. The term was shortened to "malaria" in the 20th century. C. Laveran in 1880 was the first to identify the parasites in human blood. In 1889, R. Ross discovered that mosquitoes transmitted malaria. Of the four common species that cause malaria, the most serious type is Plasmodium falciparum malaria. It can be life-threatening. However, another relatively new species, Plasmodium knowlesi, is also a dangerous species that is typically found only in long-tailed and pigtail macaque monkeys. Like P. falciparum, P. knowlesi may be deadly to anyone infected. The other three common species of malaria (P. vivax, P. malariae, and P. ovale) are generally less serious and are usually not life-threatening. It is possible to be infected with more than one species of Plasmodium at the same time.
Currently, about 2 million deaths per year worldwide are due to Plasmodium infections. The majority occur in children under 5 years of age in sub-Saharan African countries. There are about 400 million new cases per year worldwide. Most people diagnosed in the U.S. obtained their infection outside of the country, usually while living or traveling through an area where malaria is endemic.

symptoms and signs

The symptoms characteristic of malaria include flulike illness with fever, chills, muscle aches, and headache. Some patients develop nausea, vomiting, cough, and diarrhea. Cycles of chills, fever, and sweating that repeat every one, two, or three days are typical. There can sometimes be vomiting, diarrhea, coughing, and yellowing (jaundice) of the skin and whites of the eyes due to destruction of red blood cells and liver cells.
People with severe P. falciparum malaria can develop bleeding problems, shock, liver or kidney failure, central nervous system problems, coma, and can die from the infection or its complications. Cerebral malaria (coma, or altered mental status or seizures) can occur with severe P. falciparum infection. It is lethal if not treated quickly; even with treatment, about 15%-20% die.

transmitted

The life cycle of the malaria parasite (Plasmodium) is complicated and involves two hosts, humans and Anopheles mosquitoes. The disease is transmitted to humans when an infected Anopheles mosquito bites a person and injects the malaria parasites (sporozoites) into the blood. This is shown in Figure 1, where the illustration shows a mosquito taking a blood meal (circle label 1 in Figure 1).

Figure 1: CDC illustration of the life cycles of malaria parasites, Plasmodium spp. SOURCE: CDC

Sporozoites travel through the bloodstream to the liver, mature, and eventually infect the human red blood cells. While in red blood cells, the parasites again develop until a mosquito takes a blood meal from an infected human and ingests human red blood cells containing the parasites. Then the parasites reach the Anopheles mosquito's stomach and eventually invade the mosquito salivary glands. When an Anopheles mosquito bites a human, these sporozoites complete and repeat the complex Plasmodium life cycle. P. ovale and P. vivax can further complicate the cycle by producing dormant stages (hypnozoites) that may not develop for weeks to years.

particular problem

Malaria is a particular problem and a major one in areas of Asia, Africa, and Central and South America. Unless precautions are taken, anyone living in or traveling to a country where malaria is present can get the disease. Malaria occurs in about 100 countries; approximately 40% of the world population is at risk for contracting malaria.
HIV (AIDS) and malaria co-infection is a significant problem across Asia and sub-Saharan Africa. Research suggests that malaria and HIV co-infection can lead to worse clinical outcomes in patients. It seems that co-infections enhance the disease process of both pathogens.

the incubation period for malaria

The period between the mosquito bite and the onset of the malarial illness is usually one to three weeks (seven to 21 days). This initial time period is highly variable as reports suggest that the range of incubation periods may range from four days to one year. The usual incubation period may be increased when a person has taken an inadequate course of malaria prevention medications. Certain types of malaria (P. vivax and P. ovale) parasites can also take much longer, as long as eight to 10 months, to cause symptoms. These parasites remain dormant (inactive or hibernating) in the liver cells during this time. Unfortunately, some of these dormant parasites can remain even after a patient recovers from malaria, so the patient can get sick again. This situation is termed relapsing malaria.

diagnosed

Clinical symptoms associated with travel to countries that have identified malarial risk (listed above) suggest malaria as a diagnosis. Malaria tests are not routinely ordered by most physicians so recognition of travel history is essential. Unfortunately, many diseases can mimic symptoms of malaria (for example, yellow fever, dengue fever, typhoid fever, cholera, filariasis, and even measles and tuberculosis). Consequently, physicians need to order the correct special tests to diagnose malaria, especially in industrialized countries where malaria is seldom seen. Without the travel history, it is likely that other tests will be ordered initially. In addition, the long incubation periods may tend to allow people to forget the initial exposure to infected mosquitoes.
The classic and most used diagnostic test for malaria is the blood smear on a microscope slide that is stained (Giemsa stain) to show the parasites inside red blood cells (see Figure 2).

Figure 2: CDC slide of a Giemsa stained smear of red blood cells showing Plasmodium malariae and Plasmodium falciparum parasites. SOURCE: CDC/Steven Glenn, Laboratory & Consultation Division

Although this test is easily done, correct results are dependent on the technical skill of the lab technician who prepares and examines the slides with a microscope. Other tests based on immunologic principles exist; including RDTs (rapid diagnostic tests) approved for use in the U.S. in 2007 and polymerase chain reaction (PCR) tests. These are not yet widely available and are more expensive than the traditional Giemsa blood smear. Some investigators suggest such immunologic based tests be confirmed with a Giemsa blood smear.

treatment for malaria

Three main factors determine treatments: the infecting species of Plasmodium parasite, the clinical situation of the patient (for example, adult, child, or pregnant female with either mild or severe malaria), and the drug susceptibility of the infecting parasites. Drug susceptibility is determined by the geographic area where the infection was acquired. Different areas of the world have malaria types that are resistant to certain medications. The correct drugs for each type of malaria must be prescribed by a doctor who is familiar with malaria treatment protocols. Since people infected with P. falciparum malaria can die (often because of delayed treatment), immediate treatment for P. falciparum malaria is necessary.
Mild malaria can be treated with oral medication; severe malaria (one or more symptoms of either impaired consciousness/coma, severe anemia, renal failure, pulmonary edema, acute respiratory distress syndrome, shock, disseminated intravascular coagulation, spontaneous bleeding, acidosis, hemoglobinuria [hemoglobin in the urine], jaundice, repeated generalized convulsions, and/or parasitemia [parasites in the blood] of > 5%) requires intravenous (IV) drug treatment and fluids in the hospital.
Drug treatment of malaria is not always easy. Chloroquine phosphate (Aralen) is the drug of choice for all malarial parasites except for chloroquine-resistant Plasmodium strains. Although almost all strains of P. malariae are susceptible to chloroquine, P. falciparum, P. vivax, and even some P. ovale strains have been reported as resistant to chloroquine. Unfortunately, resistance is usually noted by drug-treatment failure in the individual patient. There are, however, multiple drug-treatment protocols for treatment of drug-resistant Plasmodium strains (for example, quinine sulfate plus doxycycline [Vibramycin, Oracea, Adoxa, Atridox] or tetracycline [Achromycin], or clindamycin [Cleocin], or atovaquone-proguanil [Malarone]). There are specialized labs that can test the patient's parasites for resistance, but this is not done frequently. Consequently, treatment is usually based on the majority of Plasmodium species diagnosed and its general drug-resistance pattern for the country or world region where the patient became infested. For example, P. falciparum acquired in the Middle East countries is usually susceptible to chloroquine, but if it's acquired in sub-Sahara African countries, it's usually resistant to chloroquine. The WHO's treatment policy, recently established in 2006, is to treat all cases of uncomplicated P. falciparum malaria with artemisinin-derived combination therapy (ACTs). ACTs are drug combinations (for example, artesunate-amodiaquine, artesunate-mefloquine, artesunate-pyronaridine, dihydroartemisinin-piperaquine, and chlorproguanil-dapsoneartesunate) used to treat drug-resistant P. falciparum. Unfortunately, as of 2009, a number of P. falciparum-infected individuals have parasites resistant to ACT drugs.
New drug treatments of malaria are currently under study because Plasmodium species continue to produce resistant strains that frequently spread to other areas. One promising drug class under investigation is the spiroindolones, which have been effective in stopping P. falciparum experimental infections.

people avoid getting malaria

If people must travel to an area known to have malaria, they need to find out which medications to take, and take them as prescribed. Current CDC recommendations suggest individuals begin taking antimalarial drugs about one to two weeks before traveling to a malaria infested area and for four weeks after leaving the area (prophylactic or preventative therapy). Doctors, travel clinics, or the health department can advise individuals as to what medicines to take to keep from getting malaria. Currently, there is no vaccine available for malaria, but researchers are trying to develop one.
Avoid travel to or through countries where malaria occurs if possible. If people must go to areas where malaria occurs, they should take all of the prescribed preventive medicine. In addition, the 2010 CDC international travel recommendations suggest the following precautions be taken in malaria and other disease-infested areas of the world; the following CDC recommendations are not unique for malaria but are posted by the CDC in their malarial prevention publication.

• Avoid outbreaks: To the extent possible, travelers should avoid traveling in areas of known malaria outbreaks. The CDC Travelers' Health web page provides alerts and information on regional disease transmission patterns and outbreak alerts (http://www.cdc.gov/travel).
• Be aware of peak exposure times and places: Exposure to arthropod bites may be reduced if travelers modify their patterns of activity or behavior. Although mosquitoes may bite at any time of day, peak biting activity for vectors of some diseases (for example, dengue, chikungunya) is during daylight hours. Vectors of other diseases (for example, malaria) are most active in twilight periods (for example, dawn and dusk) or in the evening after dark. Avoiding the outdoors or focusing preventive actions during peak hours may reduce risk.
• Wear appropriate clothing: Travelers can minimize areas of exposed skin by wearing long-sleeved shirts, long pants, boots, and hats. Tucking in shirts and wearing socks and closed shoes instead of sandals may reduce risk. Repellents or insecticides such as permethrin can be applied to clothing and gear for added protection; this measure is discussed in detail below.
• Check for ticks: Travelers should be advised to inspect themselves and their clothing for ticks during outdoor activity and at the end of the day. Prompt removal of attached ticks can prevent some infections.
• Bed nets: When accommodations are not adequately screened or air conditioned, bed nets are essential to provide protection and to reduce discomfort caused by biting insects. If bed nets do not reach the floor, they should be tucked under mattresses. Bed nets are most effective when they are treated with an insecticide or repellent such as permethrin. Pretreated, long-lasting bed nets can be purchased prior to traveling, or nets can be treated after purchase. The permethrin will be effective for several months if the bed net is not washed. (Long-lasting pretreated nets may be effective for much longer.)
• Insecticides: Aerosol insecticides, vaporizing mats, and mosquito coils can help to clear rooms or areas of mosquitoes; however, some products available internationally may contain pesticides that are not registered in the United States. Insecticides should always be used with caution, avoiding direct inhalation of spray or smoke.
• Optimum protection can be provided by applying repellents. The CDC recommended insect repellent should contain up to 50% DEET (N,N-diethyl-m-toluamide), which is the most effective mosquito repellent for adults and children over 2 months of age

reference :
 http://www.medicinenet.com/malaria/

KANKER SERVIKS

Penyebab Kanker Serviks

Kanker serviks merupakan jenis kanker yang paling banyak nomor tiga di dunia. Bahkan di Indonesia saja, setiap satu jam seorang wanita meninggal karena kanker ini. Kanker servik disebut juga "silent killer" karena perkembangan kanker ini sangat sulit dideteksi. Perjalanan dari infeksi virus menjadi kanker membutuhkan waktu cukup lama, sekitar 10-20 tahun. Proses ini seringkali tidak disadari hingga kemudian sampai pada tahap pra-kanker tanpa gejala. Oleh karena itu pengertian kanker serviks mutlak dipahami oleh kaum wanita di Indonesia.

Penyebab utama kanker serviks adalah infeksi Human Papilloma Virus (HPV atau virus papiloma manusia). Sekitar 70% kejadian kanker serviks merupakan akibat dari HPV 16 dan HPV 18. Awalnya sel kanker berkembang dari serviks / mulut rahim yang letaknya berada di bawah rahim dan di atas vagina. Oleh sebab itu kanker serviks disebut juga kanker leher rahim atau kanker mulut rahim. Di mulut rahim ada dua jenis sel, yaitu sel kolumnar dan sel skuamosa. Sel skuamus ini sangat berperan dalam perkembangan kanker serviks. Lihat gambar di bawah untuk mendapat gambaran tentang stadium kanker serviks:

Kanker serviks dapat terjadi jika infeksi HPV tidak sembuh dalam waktu yang lama. Apalagi dengan sistem imun atau kekebalan tubuh yang rendah, infeksi akan mengganas dan menyebabkan sel kanker. Virus ini dapat menyebar melalui sentuhan: misalnya, ada virus HPV di tangan Anda, lalu Anda menyentuh daerah genital, maka daerah serviks Anda dapat terinfeksi. Atau bisa juga dari kloset di WC umum yang sudah terkontaminasi virus (jadi sebelum duduk, Anda harus selalu membersihkan dengan alkohol). Selain itu, ada sejumlah faktor risiko atau penyebab kanker serviks:

• Wanita berusia di atas 40 tahun lebih rentan terkena kanker serviks. Semakin tua maka semakin tinggi risiko.
• Faktor genetik tidak terlalu berperan dalam terjadinya kanker serviks. Namun hal ini bukan berarti jika keluarga Anda bebas kanker serviks maka Anda tidak akan terkena! Anda harus tetap berhati-hati dan melakukan tindakan pencegahan.
• Hubungan seksual di usia yang terlalu muda, berganti-ganti partner seks, atau berhubungan seks dengan pria yang sering berganti pasangan. Virus HPV dapat menular melalui hubungan seksual. Seandainya seorang pria berhubungan seks dengan seorang wanita yang menderita kanker servik, kemudian pria tersebut berhubungan sex dengan Anda, maka virus HPV dapat menular dan menginfeksi Anda.
• Memiliki terlalu banyak anak (lebih dari 5 anak). Pada saat Anda melahirkan secara alami, janin akan melewati serviks dan menimbulkan trauma pada serviks, yang dapat memicu aktifnya sel kanker. Semakin sering janin melewati serviks, semakin sering trauma terjadi, semakin tinggi resiko kanker serviks.
• Keputihan yang berlangsung terus-menerus dan tidak diobati. Ada dua macam keputihan, yaitu normal dan tidak normal. Pada keputihan yang normal, lendir berwarna bening, tidak bau dan tidak gatal. Jika salah satu dari ketiga syarat tersebut tidak terpenuhi, artinya keputihan Anda tidak normal. Segera konsultasi dengan dokter!
• Membasuh atau membersihkan genital dengan air yang tidak bersih, misalnya air sungai atau air di toilet umum yang tidak terawat. Air yang kotor banyak mengandung kuman dan bakteri.
• Pemakaian pembalut wanita yang mengandung bahan dioksin (bahan pemutih yang dipakai untuk memutihkan pembalut hasil daur ulang dari barang bekas).
• Daya tahan tubuh yang lemah, kurangnya konsumsi vitamin C, vitamin E dan asam folat. Kebiasaan merokok juga menambah risiko kanker serviks.

Ciri dan Tanda Kanker Serviks

Pada stadium dini, gejala kanker serviks tidak terlalu kentara. Butuh waktu 10-20 tahun dari infeksi untuk menjadi kanker. Walau demikian, ciri-ciri berikut dapat dijadikan tanda kanker serviks:

• Terasa sakit saat berhubungan seksual,
• Mengeluarkan sedikit darah setelah melakukan hubungan badan,
• Keluar darah yang berlebihan saat menstruasi,
• Keputihan yang tidak normal (berwarna tidak bening, bau atau gatal),
• Pada stadium lanjut: kurang nafsu makan, sakit punggung atau tidak bisa berdiri tegak, sakit di otot bagian paha, salah satu paha bengkak, berat badan naik-turun, tidak dapat buang air kecil, bocornya urin / air seni dari vagina, pendarahan spontan setelah masa menopause, tulang yang rapuh dan nyeri panggul.

Infeksi HPV memang tidak mengakibatkan gejala yang kentara. Selain memperhatikan tanda-tanda kanker serviks di atas, ada baiknya Anda melakukan deteksi kanker serviks sejak dini. Ada sejumlah metode untuk mendeteksi atau mengetahui apakah Anda terkena kanker servik, antara lain:

• IVA - Inspeksi Visual dengan Asam asetat. Merupakan deteksi dini yang dapat Anda lakukan di klinik. Caranya dengan mengoleskan larutan asam asetat 3%-5% ke leher rahim, kemudian mengamati apakah ada perubahan warna, misalnya muncul bercak putih. Jika ada, berarti kemungkinan terdapat infeksi pada serviks dan harus dilakukan pemeriksaaan lanjutan.
• Pap Smear atau dikenal juga dengan sebutan Papanicolaou test, Pap test, cervical smear, smear test. Pemeriksaan pap smear memiliki berbagai kelebihan: biaya murah, waktu cepat dan hasil akurat. Tes ini dapat dilakukan kapan saja kecuali saat masa haid atau menstruasi; setidaknya satu tahun sekali. Pemeriksaan dilakukan di atas meja periksa kandungan oleh dokter/bidan yang sudah terlatih dengan menggunakan spekulum untuk membantu membuka alat kelamin wanita. Setelah vagina terbuka, bagian leher rahim diusap dengan spatula secara melingkar untuk mengambil contoh sel endoserviks. Kemudian hasil usapan tersebut diperiksa dengan mikroskop untuk mengetahui apakah ada sel abnormal, infeksi atau radang. Melakukan pap smear secara teratur dapat mengurangi risiko kematian akibat kanker serviks.
• Thin prep merupakan metode berbasis cairan yang lebih akurat dari pap smear, karena pap smear hanya mengambil sebagian sel dari leher rahim, sedangkan thin prep memeriksa seluruh bagian serviks. Sampel yang diambil dari leher rahim dimasukkan ke dalam vial / botol yang berisi cairan, kemudian dibawa ke laboratorium untuk diperiksa. Di lab, sampel tersebut dijadikan slide dan diberi pewarna khusus agar lebih jelas. Membran khusus digunakan untuk membuat preparat dengan irisan tipis, yang akan memperlihatkan infeksi atau jaringan abnormal. Tingkat akurasi metode ini hampir mencapai 100%.

Pencegahan dan Pengobatan Kanker Serviks

Mencegah lebih baik daripada mengobati. Oleh karena itu, sebelum Anda terkena kanker serviks, ikuti saran berikut untuk mencegah infeksi virus HPV:

• Jaga kesehatan dan daya tahan tubuh dengan cara konsumsi makanan bergizi. Jalani pola hidup sehat dengan cara makan sayuran, buah dan sereal. Perbanyak makanan yang mengandung vitamin A, C dan E serta asam folat untuk mengurangi risiko kanker leher rahim.
• Sebelum menggunakan toilet di tempat umum, selalu bersihkan bibir kloset dengan alkohol. Jangan membersihkan genital dengan air kotor.
• Hindari hubungan seks di usia dini. Hindari berhubungan badan dengan banyak partner karena HPV menular melalui hubungan seksual. Hindari berhubungan sex selama masa haid/menstruasi.
• Hindari merokok, karena penggunaan tembakau dapat menyebabkan kanker.
• Rutin melakukan screening berupa pap smear atau IVA untuk deteksi kanker serviks secara dini.
• Vaksinasi dapat dilakukan pada perempuan usia 10-55 tahun dengan jadwal suntikan sebanyak 3 kali, yaitu pada bulan 0, 1 dan 6. Vaksin HPV akan meningkatkan daya imun anak sehingga lebih resistan terhadap virus.

Jika Anda sudah dideteksi menderita kanker serviks, jangan khawatir. Sekarang ini sudah ada sejumlah metode untuk mengobati kanker serviks. Pada stadium awal, pengobatan kanker serviks dilakukan dengan cara menyingkirkan bagian yang sudah terkena kanker. Misalnya dengan pembedahan listrik, laser atau cyrosurgery (membekukan dan membuang jaringan abnormal).
Untuk pengobatan kanker serviks stadium lanjut, dilakukan terapi kemoterapi dan radioterapi. Pada stadium akhir atau kasus yang parah maka terpaksa dilakukan histerektomi, yaitu bedah pengangkatan rahim (uterus) secara total agar sel-sel kanker yang sudah berkembang dalam kandungan tidak menyebar ke bagian lain dalam tubuh.

Sumber :
 http://kankerserviks.org/

 

Polimiositis 

 

Deskripsi

Polimiositis adalah penyakit inflamasi pada otot yang terus-menerus dan menyebabkan kelemahan otot rangka, yang mengendalikan gerakan. Secara medis, polimiositis diklasifikasikan sebagai miopati inflamasi kronis. Polimiositis dapat terjadi pada semua usia, tetapi sebagian besar mempengaruhi orang dewasa dengan usia 40 sampai 50-an tahun. Penyakit ini lebih sering terjadi pada orang kulit hitam dibandingkan kulit putih, dan wanita lebih sering terpengaruh daripada pria.

Penyebab

Penyebab pasti dari polimiositis belum diketahui, tetapi karakteristik penyakit ini sama dengan gangguan autoimun, dimana sistem kekebalan tubuh menyerang komponen tubuh normal. Biasanya, sistem kekebalan tubuh bekerja untuk melindungi sel sehat dari serangan benda asing, seperti bakteri dan virus. Polimiositis biasanya mempengaruhi otot-otot yang paling dekat dengan batang, terutama di pinggul, paha, bahu, lengan atas dan leher. Jika Anda menderita polimiositis, sebuah penyebab yang tidak diketahui dapat bertindak sebagai pemicu sistem kekebalan tubuh untuk mulai memproduksi antibodi autoimun (autoantibodi) yang menyerang jaringan tubuh sendiri. Banyak orang yang menderita polimiositis menunjukkan tingkat terdeteksi autoantibodi dalam darahnya.

Gejala

Tanda dan gejala polimiositis muncul secara bertahap, sehingga mungkin sulit untuk mendeteksi lebih dini. Penyakit ini juga dapat berfluktuasi dari minggu ke minggu atau bulan ke bulan. P Polimiositis dapat memburuk dari waktu ke waktu dan membuat Anda mungkin kesulitan naik tangga, bangkit dari posisi duduk, mengangkat benda sampai di atas kepala. Polimiositis ditandai dengan gejala sebagai berikut: 1. kelemahan otot progresif 2. Kesulitan menelan (disfagia) 3. Kesulitan berbicara 4. Ringan sendi atau nyeri tekan otot 5. Kelelahan 6. Sesak napas

Pengobatan

Jika Anda mengembangkan tanda dan gejala yang berhubungan dengan polimiositis, pergilah ke dokter untuk evaluasi dan diagnosis. Meskipun tidak ada obat untuk polimiositis, pengobatan seperti kortikosteroid dan terapi dapat meningkatkan kekuatan dan fungsi otot. Kortikosteroid adalah pengobatan dengan obat-obat yang menekan sistem kekebalan tubuh, membatasi produksi antibodi dan mengurangi peradangan otot. Sumber: MayoClinic

Meningioma 

 Deskripsi

Meningioma merupakan tumor yang tumbuh dari meninges, selaput yang melindungi otak dan sumsum tulang belakang. Kebanyakan meningioma diklasifikasikan sebagai tumor yang tidak tidak jinak maupun ganas. Meningioma biasanya terjadi pada wanita yang lebih tua. Namun bisa juga terjadi pada pria usia berapapun, termasuk anak-anak.

Penyebab

Penyebab meningioma belum jelas namun diketahui ada sesuatu yang mengubah beberapa sel di selaput meninges sehingga berkembang biak secara berlebihan dan membentuk tumor. Namun penyebab perubahan itu masih belum ditemukan.

Gejala

1. Perubahan penglihatan seperti melihat ganda atau buram 2. Sakit kepala yang semakin lama semakin memburuk 3. Kehilangan pendengaran 4. Kehilangan daya ingat 5. Kejang 6. Lengan atau kaki terasa lemas

Pengobatan

1. Jika meningioma-nya tidak terlalu parah atau tumbuh secara perlahan, Anda hanya perlu melakukan pemindaian otak secara teratur. 2. Operasi 3. Terapi radiasi 4. Radiosurgery 5. Fractionated radiation 6. Obat seperti hydroxyurea

http://health.detik.com/readpenyakit/959/meningioma?mode_op=deskripsi

Infections of the Respiratory System

1. Upper Respiratory Infections: Common Cold, Sinusitis, Pharyngitis, Epiglottitis and Laryngotracheitis

Etiology: Most upper respiratory infections are of viral etiology. Epiglottitis and laryngotracheitis are exceptions with severe cases likely caused by Haemophilus influenzae type b. Bacterial pharyngitis is often caused by Streptococcus pyogenes

Pathogenesis: Organisms gain entry to the respiratory tract by inhalation of droplets and invade the mucosa. Epithelial destruction may ensue, along with redness, edema, hemorrhage and sometimes an exudate.

Clinical Manifestations: Initial symptoms of a cold are runny, stuffy nose and sneezing, usually without fever. Other upper respiratory infections may have fever. Children with epiglottitis may have difficulty in breathing, muffled speech, drooling and stridor. Children with serious laryngotracheitis (croup) may also have tachypnea, stridor and cyanosis.

Microbiologic Diagnosis: Common colds can usually be recognized clinically. Bacterial and viral cultures of throat swab specimens are used for pharyngitis, epiglottitis and laryngotracheitis. Blood cultures are also obtained in cases of epiglottitis.

Prevention and Treatment: Viral infections are treated symptomatically. Streptococcal pharyngitis and epiglottitis caused by H influenzae are treated with antibacterials. Haemophilus influenzae type b vaccine is commercially available and is now a basic component of childhood immunization program.

2. Lower Respiratory Infections: Bronchitis, Bronchiolitis and Pneumonia

Etiology: Causative agents of lower respiratory infections are viral or bacterial. Viruses cause most cases of bronchitis and bronchiolitis. In community-acquired pneumonias, the most common bacterial agent is Streptococcus pneumoniae. Atypical pneumonias are cause by such agents as Mycoplasma pneumoniae, Chlamydia spp, Legionella, Coxiella burnetti and viruses. Nosocomial pneumonias and pneumonias in immunosuppressed patients have protean etiology with gram-negative organisms and staphylococci as predominant organisms.

Pathogenesis: Organisms enter the distal airway by inhalation, aspiration or by hematogenous seeding. The pathogen multiplies in or on the epithelium, causing inflammation, increased mucus secretion, and impaired mucociliary function; other lung functions may also be affected. In severe bronchiolitis, inflammation and necrosis of the epithelium may block small airways leading to airway obstruction.

Clinical Manifestations: Symptoms include cough, fever, chest pain, tachypnea and sputum production. Patients with pneumonia may also exhibit non-respiratory symptoms such as confusion, headache, myalgia, abdominal pain, nausea, vomiting and diarrhea.

Microbiologic Diagnosis: Sputum specimens are cultured for bacteria, fungi and viruses. Culture of nasal washings is usually sufficient in infants with bronchiolitis. Fluorescent staining technic can be used for legionellosis. Blood cultures and/or serologic methods are used for viruses, rickettsiae, fungi and many bacteria. Enzyme-linked immunoassay methods can be used for detections of microbial antigens as well as antibodies. Detection of nucleotide fragments specific for the microbial antigen in question by DNA probe or polymerase chain reaction can offer a rapid diagnosis.

Prevention and Treatment: Symptomatic treatment is used for most viral infections. Bacterial pneumonias are treated with antibacterials. A polysaccharide vaccine against 23 serotypes of Streptococcus pneumoniae is recommended for individuals at high risk.

Upper Respiratory Infections

Infections of the respiratory tract are grouped according to their symptomatology and anatomic involvement. Acute upper respiratory infections (URI) include the common cold, pharyngitis, epiglottitis, and laryngotracheitis. These infections are usually benign, transitory and self-limited, altho ugh epiglottitis and laryngotracheitis can be serious diseases in children and young infants. Etiologic agents associated with URI include viruses, bacteria, mycoplasma and fungi. Respiratory infections are more common in the fall and winter when school starts and indoor crowding facilitates transmission. 

 

 

Common Cold

Etiology

Common colds are the most prevalent entity of all respiratory infections and are the leading cause of patient visits to the physician, as well as work and school absenteeism. Most colds are caused by viruses. Rhinoviruses with more than 100 serotypes are the most common pathogens, causing at least 25% of colds in adults. Coronaviruses may be responsible for more than 10% of cases. Parainfluenza viruses, respiratory syncytial virus, adenoviruses and influenza viruses have all been linked to the common cold syndrome. All of these organisms show seasonal variations in incidence. The cause of 30% to 40% of cold syndromes has not been determined.

Pathogenesis

The viruses appear to act through direct invasion of epithelial cells of the respiratory mucosa, but whether there is actual destruction and sloughing of these cells or loss of ciliary activity depends on the specific organism involved. There is an increase in both leukocyte infiltration and nasal secretions, including large amounts of protein and immunoglobulin, suggesting that cytokines and immune mechanisms may be responsible for some of the manifestations of the common cold.

Pathogenesis of viral and bacterial mucosal respiratory infections. 


Pathogenesis of upper respiratory tract infections.

Clinical Manifestations

After an incubation period of 48–72 hours, classic symptoms of nasal discharge and obstruction, sneezing, sore throat and cough occur in both adults and children. Myalgia and headache may also be present. Fever is rare. The duration of symptoms and of viral shedding varies with the pathogen and the age of the patient. Complications are usually rare, but sinusitis and otitis media may follow.

Microbiologic Diagnosis

The diagnosis of a common cold is usually based on the symptoms (lack of fever combined with symptoms of localization to the nasopharynx). Unlike allergic rhinitis, eosinophils are absent in nasal secretions. Although it is possible to isolate the viruses for definitive diagnosis, that is rarely warranted.

Prevention and Treatment

Treatment of the uncomplicated common cold is generally symptomatic. Decongestants, antipyretics, fluids and bed rest usually suffice. Restriction of activities to avoid infecting others, along with good hand washing, are the best measures to prevent spread of the disease. No vaccine is commercially available for cold prophylaxis.

Sinusitis

Sinusitis is an acute inflammatory condition of one or more of the paranasal sinuses. Infection plays an important role in this affliction. Sinusitis often results from infections of other sites of the respiratory tract since the paranasal sinuses are contiguous to, and communicate with, the upper respiratory tract.

Etiology

Acute sinusitis most often follows a common cold which is usually of viral etiology. Vasomotor and allergic rhinitis may also be antecedent to the development of sinusitis. Obstruction of the sinusal ostia due to deviation of the nasal septum, presence of foreign bodies, polyps or tumors can predispose to sinusitis. Infection of the maxillary sinuses may follow dental extractions or an extension of infection from the roots of the upper teeth. The most common bacterial agents responsible for acute sinusitis are Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis. Other organisms including Staphylococcus aureus, Streptococcus pyogenes, gram-negative organisms and anaerobes have also been recovered. Chronic sinusitis is commonly a mixed infection of aerobic and anaerobic organisms.

Pathogenesis

Infections caused by viruses or bacteria impair the ciliary activity of the epithelial lining of the sinuses and increased mucous secretions. This leads to obstruction of the paranasal sinusal ostia which impedes drainage. With bacterial multiplication in the sinus cavities, the mucus is converted to mucopurulent exudates. The pus further irritates the mucosal lining causing more edema, epithelial destruction and ostial obstruction. When acute sinusitis is not resolved and becomes chronic, mucosal thickening results and the development of mucoceles and polyps may ensue.

Clinical Manifestations

The maxillary and ethmoid sinuses are most commonly involved in sinusitis. The frontal sinuses are less often involved and the sphenoid sinuses are rarely affected. Pain, sensation of pressure and tenderness over the affected sinus are present. Malaise and low grade fever may also occur. Physical examination usually is not remarkable with no more than an edematous and hyperemic nasal mucosa.
In uncomplicated chronic sinusitis, a purulent nasal discharge is the most constant finding. There may not be pain nor tenderness over the sinus areas. Thickening of the sinus mucosa and a fluid level are usually seen in x-ray films or magnetic resonance imaging.

Microbiologic Diagnosis

For acute sinusitis, the diagnosis is made from clinical findings. A bacterial culture of the nasal discharge can be taken but is not very helpful as the recovered organisms are generally contaminated by the resident flora from the nasal passage. In chronic sinusitis, a careful dental examination, with sinus x-rays may be required. An antral puncture to obtain sinusal specimens for bacterial culture is needed to establish a specific microbiologic diagnosis.

Prevention and Treatment

Symptomatic treatment with analgesics and moist heat over the affected sinus pain and a decongestant to promote sinus drainage may suffice. For antimicrobial therapy, a beta-lactamase resistant antibiotic such as amoxicillin-clavulanate or a cephalosporin may be used. For chronic sinusitis, when conservative treatment does not lead to a cure, irrigation of the affected sinus may be necessary. Culture from an antral puncture of the maxillary sinus can be performed to identify the causative organism for selecting antimicrobial therapy. Specific preventive procedures are not available. Proper care of infectious and/or allergic rhinitis, surgical correction to relieve or avoid obstruction of the sinusal ostia are important. Root abscesses of the upper teeth should receive proper dental care to avoid secondary infection of the maxillary sinuses.

Otitis

Infections of the ears are common events encountered in medical practice, particularly in young children. Otitis externa is an infection involving the external auditory canal while otitis media denotes inflammation of the middle ear.

Etiology

For otitis externa, the skin flora such as Staphylococcus epidermidis, Staphylococcus aureus, diphtheroids and occasionally an anaerobic organism, Propionibacterium acnes are major etiologic agents. In a moist and warm environment, a diffuse acute otitis externa (Swimmer's ear) may be caused by Pseudomonas aeruginosa, along with other skin flora. Malignant otitis externa is a severe necrotizing infection usually caused by Pseudomonas aeruginosa.
For otitis media, the commonest causative bacteria are Streptococcus pneumoniae, Hemophilus influenzae and beta-lactamase producing Moraxella catarrhalis. Respiratory viruses may play a role in otitis media but this remains uncertain. Mycoplasma pneumoniae has been reported to cause hemorrhagic bullous myringitis in an experimental study among nonimmune human volunteers inoculated with M pneumoniae. However, in natural cases of M pneumoniae infection, clinical bullous myringitis or otitis media is uncommon.

Pathogenesis

The narrow and tortuous auditory canal is lined by a protective surface epithelium. Factors that may disrupt the natural protective mechanisms, such as high temperature and humidity, trauma, allergy, tissue maceration, removal of cerumen and an alkaline pH environment, favor the development of otitis externa. Prolonged immersion in a swimming pool coupled with frequent ear cleansing increases the risk of otitis externa.
Acute otitis media commonly follows an upper respiratory infection extending from the nasopharynx via the eustachian tube to the middle ear. Vigorous nose blowing during a common cold, sudden changes of air pressure, and perforation of the tympanic membrane also favor the development of otitis media. The presence of purulent exudate in the middle ear may lead to a spread of infection to the inner ear and mastoids or even meninges

Clinical Manifestations

Otitis externa

Furuncles of the external ear, similar to those in skin infection, can cause severe pain and a sense of fullness in the ear canal. When the furuncle drains, purulent otorrhea may be present. In generalized otitis externa, itching, pain and tenderness of the ear lobe on traction are present. Loss of hearing may be due to obstruction of the ear canal by swelling and the presence of purulent debris.
Malignant otitis externa tends to occur in elderly diabetic patients. It is characterized by severe persistent earache, foul smelling purulent discharge and the presence of granulation tissue in the auditory canal. The infection may spread and lead to osteomyelitis of the temporal bone or externally to involve the pinna with osteochondritis.

Otitis media

Acute otitis media occurs most commonly in young children. The initial complaint usually is persistent severe earache (crying in the infant) accompanied by fever, and, and vomiting. Otologic examination reveals a bulging, erythematous tympanic membrane with loss of light reflex and landmarks. If perforation of the tympanic membrane occurs, serosanguinous or purulent discharge may be present. In the event of an obstruction of the eustachian tube, accumulation of a usually sterile effusion in the middle ear results in serous otitis media. Chronic otitis media frequently presents a permanent perforation of the tympanic membrane. A central perforation of the pars tensa is more benign. On the other hand, an attic perforation of the pars placcida and marginal perforation of the pars tensa are more dangerous and often associated with a cholesteatoma.

Diagnosis

The diagnosis of both otitis externa and otitis media can be made from history, clinical symptomatology and physical examinations. Inspection of the tympanic membrane is an indispensable skill for physicians and health care workers. All discharge, ear wax and debris must be removed and to perform an adequate otoscopy. In the majority of patients, routine cultures are not necessary, as a number of good bacteriologic studies have shown consistently the same microbial pathogens mentioned in the section of etiology. If the patient is immunocompromised or is toxic and not responding to initial antimicrobial therapy tympanocentesis (needle aspiration) to obtain middle ear effusion for microbiologic culture is indicated.

Prevention and Treatment

Otitis externa

Topical therapy is usually sufficient and systemic antimicrobials are seldom needed unless there are signs of spreading cellulitis and the patient appears toxic. A combination of topical antibiotics such as neomycin sulfate, polymyxin B sulfate and corticosteroids used as eardrops, is a preferred therapy. In some cases, acidification of the ear canal by applying a 2% solution of acetic acid topically may also be effective. If a furuncle is present in the external canal, the physician should allow it to drain spontaneously.

Otitis media

Amoxicillin is an effective and preferred antibiotic for treatment of acute otitis media. Since beta-lactamase producing H influenzae and M catarrhalis can be a problem in some communities, amoxicillin-clavulanate is used by many physicians. Oral preparations of trimethoprim/sulfamethoxazole, second and third generation cephalosporins, tetracyclines and macrolides can also be used. When there is a large effusion, tympanocentesis may hasten the resolution process by decreasing the sterile effusion. Patients with chronic otitis media and frequent recurrences of middle ear infections may be benefitted by chemoprophylaxis with once daily oral amoxicillin or trimethoprim/sulfamethoxazole during the winter and spring months. In those patients with persistent effusion of the middle ear, surgical interventions with myringotomy, adenoidectomy and the placement of tympanotomy tubes has been helpful.
Use of polyvalent pneumococcal vaccines has been evaluated for the prevention of otitis media in children. However, children under two years of age do not respond satisfactorily to polysaccharide antigens; further, no significant reduction in the number of middle ear infections was demonstrable. Newer vaccines composed of pneumococcal capsular polysaccharides conjugated to proteins may increase the immunogenicity and are currently under clinical investigation for efficacy and safety.

Pharyngitis

Etiology

Pharyngitis is an inflammation of the pharynx involving lymphoid tissues of the posterior pharynx and lateral pharyngeal bands. The etiology can be bacterial, viral and fungal infections as well as noninfectious etiologies such as smoking. Most cases are due to viral infections and accompany a common cold or influenza. Type A coxsackieviruses can cause a severe ulcerative pharyngitis in children (herpangina), and adenovirus and herpes simplex virus, although less common, also can cause severe pharyngitis. Pharyngitis is a common symptom of Epstein-Barr virus and cytomegalovirus infections.
Group A beta-hemolytic streptococcus or Streptococcus pyogenes is the most important bacterial agent associated with acute pharyngitis and tonsillitis. Corynebacterium diphtheriae causes occasional cases of acute pharyngitis, as do mixed anaerobic infections (Vincent's angina), Corynebacterium haemolyticum, Neisseria gonorrhoeae, and Chlamydia trachomatis. Outbreaks of Chlamydia pneumoniae (TWAR agent) causing pharyngitis or pneumonitis have occurred in military recruits. Mycoplasma pneumoniae and Mycoplasma hominis have been associated with acute pharyngitis. Candida albicans, which causes oral candidiasis or thrush, can involve the pharynx, leading to inflammation and pain.

Pathogenesis

As with common cold, viral pathogens in pharyngitis appear to invade the mucosal cells of the nasopharynx and oral cavity, resulting in edema and hyperemia of the mucous membranes and tonsils (Fig 93-2). Bacteria attach to and, in the case of group A beta-hemolytic streptococci, invade the mucosa of the upper respiratory tract. Many clinical manifestations of infection appear to be due to the immune reaction to products of the bacterial cell. In diphtheria, a potent bacterial exotoxin causes local inflammation and cell necrosis.

Clinical Manifestations

Pharyngitis usually presents with a red, sore, or “scratchy” throat. An inflammatory exudate or membranes may cover the tonsils and tonsillar pillars. Vesicles or ulcers may also be seen on the pharyngeal walls. Depending on the pathogen, fever and systemic manifestations such as malaise, myalgia, or headache may be present. Anterior cervical lymphadenopathy is common in bacterial pharyngitis and difficulty in swallowing may be present.

Microbiologic Diagnosis

The goal in the diagnosis of pharyngitis is to identify cases that are due to group A beta-hemolytic streptococci, as well as the more unusual and potentially serious infections. The various forms of pharyngitis cannot be distinguished on clinical grounds. Routine throat cultures for bacteria are inoculated onto sheep blood and chocolate agar plates. Thayer-Martin medium is used if N gonorrhoeae is suspected. Viral cultures are not routinely obtained for most cases of pharyngitis. Serologic studies may be used to confirm the diagnosis of pharyngitis due to viral, mycoplasmal or chlamydial pathogens. Rapid diagnostic tests with fluorescent antibody or latex agglutination to identify group A streptococci from pharyngeal swabs are available. Gene probe and polymerase chain reaction can be used to detect unusual organisms such as M pneumoniae, chlamydia or viruses but these procedures are not routine diagnostic methods.

Prevention and Treatment

Symptomatic treatment is recommended for viral pharyngitis. The exception is herpes simplex virus infection, which can be treated with acyclovir if clinically warranted or if diagnosed in immunocompromised patients. The specific antibacterial agents will depend on the causative organism, but penicillin G is the therapy of choice for streptococcal pharyngitis. Mycoplasma and chlamydial infections respond to erythromycin, tetracyclines and the new macrolides.

Epiglottitis and Laryngotracheitis

Etiology

Inflammation of the upper airway is classified as epiglottitis or laryngotracheitis (croup) on the basis of the location, clinical manifestations, and pathogens of the infection. Haemophilus influenzae type b is the most common cause of epiglottitis, particularly in children age 2 to 5 years. Epiglottitis is less common in adults. Some cases of epiglottitis in adults may be of viral origin. Most cases of laryngotracheitis are due to viruses. More serious bacterial infections have been associated with H influenzae type b, group A beta-hemolytic streptococcus and C diphtheriae. Parainfluenza viruses are most common but respiratory syncytial virus, adenoviruses, influenza viruses, enteroviruses and Mycoplasma pneumoniae have been implicated.

Pathogenesis

A viral upper respiratory infection may precede infection with H influenzae in episodes of epiglottitis. However, once H influenzae type b infection starts, rapidly progressive erythema and swelling of the epiglottis ensue, and bacteremia is usually present. Viral infection of laryngotracheitis commonly begins in the nasopharynx and eventually moves into the larynx and trachea. Inflammation and edema involve the epithelium, mucosa and submucosa of the subglottis which can lead to airway obstruction.

Clinical Manifestations

The syndrome of epiglottitis begins with the acute onset of fever, sore throat, hoarseness, drooling, dysphagia and progresses within a few hours to severe respiratory distress and prostration. The clinical course can be fulminant and fatal. The pharynx may be inflamed, but the diagnostic finding is a “cherry-red” epiglottis.
A history of preceding cold-like symptoms is typical of laryngotracheitis, with rhinorrhea, fever, sore throat and a mild cough. Tachypnea, a deep barking cough and inspiratory stridor eventually develop. Children with bacterial tracheitis appear more ill than adults and are at greater risk of developing airway obstruction.
Haemophilus influenzae type b is isolated from the blood or epiglottis in the majority of patients with epiglottis; therefore a blood culture should always be performed. Sputum cultures or cultures from pharyngeal swabs may be used to isolate pathogens in patients with laryngotracheitis. Serologic studies to detect a rise in antibody titers to various viruses are helpful for retrospective diagnosis. Newer, rapid diagnostic techniques, using immunofluorescent-antibody staining to detect virus in sputum, pharyngeal swabs, or nasal washings, have been successfully used. Enzyme-linked immunosorbent assay (ELISA), DNA probe and polymerase chain reaction procedures for detection of viral antibody or antigens are now available for rapid diagnosis.

Prevention and Treatment

Epiglottitis is a medical emergency, especially in children. All children with this diagnosis should be observed carefully and be intubated to maintain an open airway as soon as the first sign of respiratory distress is detected. Antibacterial therapy should be directed at H influenzae. Patients with croup are usually successfully managed with close observation and supportive care, such as fluid, humidified air, and racemic epinephrine. For prevention, Haemophilus influenzae type b conjugated vaccine is recommended for all pediatric patients, as is immunization against diphtheria.

Lower Respiratory Infections

Infections of the lower respiratory tract include bronchitis, bronchiolitis and pneumonia. These syndromes, especially pneumonia, can be severe or fatal. Although viruses, mycoplasma, rickettsiae and fungi can all cause lower respiratory tract infections, bacteria are the dominant pathogens; accounting for a much higher percentage of lower than of upper respiratory tract infections.

Bronchitis and Bronchiolitis

Etiology

Bronchitis and bronchiolitis involve inflammation of the bronchial tree. Bronchitis is usually preceded by an upper respiratory tract infection or forms part of a clinical syndrome in diseases such as influenza, rubeola, rubella, pertussis, scarlet fever and typhoid fever. Chronic bronchitis with a persistent cough and sputum production appears to be caused by a combination of environmental factors, such as smoking, and bacterial infection with pathogens such as H influenzae and S pneumoniae. Bronchiolitis is a viral respiratory disease of infants and is caused primarily by respiratory syncytial virus. Other viruses, including parainfluenza viruses, influenza viruses and adenoviruses (as well as occasionally M pneumoniae) are also known to cause bronchiolitis.

Pathogenesis

When the bronchial tree is infected, the mucosa becomes hyperemic and edematous and produces copious bronchial secretions. The damage to the mucosa can range from simple loss of mucociliary function to actual destruction of the respiratory epithelium, depending on the organisms(s) involved. Patients with chronic bronchitis have an increase in the number of mucus-producing cells in their airways, as well as inflammation and loss of bronchial epithelium, Infants with bronchiolitis initially have inflammation and sometimes necrosis of the respiratory epithelium, with eventual sloughing. Bronchial and bronchiolar walls are thickened. Exudate made up of necrotic material and respiratory secretions and the narrowing of the bronchial lumen lead to airway obstruction. Areas of air trapping and atelectasis develop and may eventually contribute to respiratory failure.

Clinical Manifestations

Symptoms of an upper respiratory tract infection with a cough is the typical initial presentation in acute bronchitis. Mucopurulent sputum may be present, and moderate temperature elevations occur. Typical findings in chronic bronchitis are an incessant cough and production of large amounts of sputum, particularly in the morning. Development of respiratory infections can lead to acute exacerbations of symptoms with possibly severe respiratory distress.
Coryza and cough usually precede the onset of bronchiolitis. Fever is common. A deepening cough, increased respiratory rate, and restlessness follow. Retractions of the chest wall, nasal flaring, and grunting are prominent findings. Wheezing or an actual lack of breath sounds may be noted. Respiratory failure and death may result.

Microbiologic Diagnosis

Bacteriologic examination and culture of purulent respiratory secretions should always be performed for cases of acute bronchitis not associated with a common cold. Patients with chronic bronchitis should have their sputum cultured for bacteria initially and during exacerbations. Aspirations of nasopharyngeal secretions or swabs are sufficient to obtain specimens for viral culture in infants with bronchiolitis. Serologic tests demonstrating a rise in antibody titer to specific viruses can also be performed. Rapid diagnostic tests for antibody or viral antigens may be performed on nasopharyngeal secretions by using fluorescent-antibody staining, ELISA or DNA probe procedures.

Prevention and Treatment

With only a few exceptions, viral infections are treated with supportive measures. Respiratory syncytial virus infections in infants may be treated with ribavirin. Amantadine and rimantadine are available for chemoprophylaxis or treatment of influenza type A viruses. Selected groups of patients with chronic bronchitis may receive benefit from use of corticosteroids, bronchodilators, or prophylactic antibiotics.

Pneumonia

Pneumonia is an inflammation of the lung parenchyma. Consolidation of the lung tissue may be identified by physical examination and chest x-ray. From an anatomical point of view, lobar pneumonia denotes an alveolar process involving an entire lobe of the lung while bronchopneumonia describes an alveolar process occurring in a distribution that is patchy without filling an entire lobe. Numerous factors, including environmental contaminants and autoimmune diseases, as well as infection, may cause pneumonia. The various infectious agents that cause pneumonia are categorized in many ways for purposes of laboratory testing, epidemiologic study and choice of therapy. Pneumonias occurring in usually healthy persons not confined to an institution are classified as community-acquired pneumonias. Infections arise while a patient is hospitalized or living in an institution such as a nursing home are called hospital-acquired or nosocomial pneumonias. Etiologic pathogens associated with community-acquired and hospital-acquired pneumonias are somewhat different. However, many organisms can cause both types of infections.


Pathogenesis of bacterial pneumonias.

Etiology

Bacterial pneumonias

Streptococcus pneumoniae is the most common agent of community-acquired acute bacterial pneumonia. More than 80 serotypes, as determined by capsular polysaccharides, are known, but 23 serotypes account for over 90% of all pneumococcal pneumonias in the United States. Pneumonias caused by other streptococci are uncommon. Streptococcus pyogenes pneumonia is often associated with a hemorrhagic pneumonitis and empyema. Community-acquired pneumonias caused by Staphylococcus aureus are also uncommon and usually occur after influenza or from staphylococcal bacteremia. Infections due to Haemophilus influenzae (usually nontypable) and Klebsiella pneumoniae are more common among patients over 50 years old who have chronic obstructive lung disease or alcoholism.
The most common agents of nosocomial pneumonias are aerobic gram-negative bacilli that rarely cause pneumonia in healthy individuals. Pseudomonas aeruginosa, Escherichia coli, Enterobacter, Proteus, and Klebsiella species are often identified. Less common agents causing pneumonias include Francisella tularensis, the agent of tularemia; Yersinia pestis, the agent of plague; and Neisseria meningitidis, which usually causes meningitis but can be associated with pneumonia, especially among military recruits. Xanthomonas pseudomallei causes melioidosis, a chronic pneumonia in Southeast Asia.
Mycobacterium tuberculosis can cause pneumonia. Although the incidence of tuberculosis is low in industrialized countries, M tuberculosis infections still continue to be a significant public health problem in the United States, particularly among immigrants from developing countries, intravenous drug abusers, patients infected with human immunodeficiency virus (HIV), and the institutionalized elderly. Atypical Mycobacterium species can cause lung disease indistinguishable from tuberculosis.

Aspiration pneumonias

Aspiration pneumonia from anaerobic organisms usually occurs in patients with periodontal disease or depressed consciousness. The bacteria involved are usually part the oral flora and cultures generally show a mixed bacterial growth. Actinomyces, Bacteroides, Peptostreptococcus, Veilonella, Propionibacterium, Eubacterium, and Fusobacterium spp are often isolated.

Atypical pneumonias

Atypical pneumonias are those that are not typical bacterial lobar pneumonias. Mycoplasma pneumoniae produces pneumonia most commonly in young people between 5 and 19 years of age. Outbreaks have been reported among military recruits and college students.
Legionella species, including L pneumophila, can cause a wide range of clinical manifestations. The 1976 outbreak in Philadelphia was manifested as a typical serious pneumonia in affected individuals, with a mortality of 17%. These organisms can survive in water and cause pneumonia by inhalation from aerosolized tap water, respiratory devices, air conditioners and showers. They also have been reported to cause nosocomial pneumonias.
Chlamydia spp noted to cause pneumonitis are C trachomatis, C psittaci and C pneumoniae. Chlamydia trachomatis causes pneumonia in neonates and young infants. C psittaci is a known cause for occupational pneumonitis in bird handlers such as turkey farmers. Chlamydia pneumoniae has been associated with outbreaks of pneumonia in military recruits and on college campuses.
Coxiella burnetii the rickettsia responsible for Q fever, is acquired by inhalation of aerosols from infected animal placentas and feces. Pneumonitis is one of the major manifestations of this systemic infection.
Viral pneumonias are rare in healthy civilian adults. An exception is the viral pneumonia caused by influenza viruses, which can have a high mortality in the elderly and in patients with underlying disease. A serious complication following influenza virus infection is a secondary bacterial pneumonia, particularly staphylococcal pneumonia. Respiratory syncytial virus can cause serious pneumonia among infants as well as outbreaks among institutionalized adults. Adenoviruses may also cause pneumonia, serotypes 1,2,3,7 and 7a have been associated with a severe, fatal pneumonia in infants. Although varicella-zoster virus pneumonitis is rare in children, it is not uncommon in individuals over 19 years old. Morality can be as high as 10% to 30%. Measles pneumonia may occur in adults.

Other pneumonias and immunosuppression

Cytomegalovirus is well known for causing congenital infections in neonates, as well as the mononucleosis-like illness seen in adults. However, among its manifestations in immunocompromised individuals is a severe and often fatal pneumonitis. Herpes simplex virus also causes a pneumonia in this population. Giant-cell pneumonia is a serious complication of measles and has been found in children with immunodeficiency disorders or underlying cancers who receive live attenuated measles vaccine. Actinomyces and Nocardia spp can cause pneumonitis, particularly in immunocompromised hosts.
Among the fungi, Cryptococcus neoformans and Sporothrix schenckii are found worldwide, whereas Blastomyces dermatitidis, Coccidioides immitis, Histoplasma capsulatum and Paracoccidioides brasiliensis have specific geographic distributions. All can cause pneumonias, which are usually chronic and possible clinically inapparent in normal hosts, but are manifested as more serious diseases in immunocompromised patients. Other fungi, such as Aspergillus and Candida spp, occasionally are responsible for pneumonias in severely ill or immunosuppressed patients and neonates.
Pneumocystis carinii produces a life-threatening pneumonia among patients immunosuppressed by acquired immune deficiency syndrome (AIDS), hematologic cancers, or medical therapy. It is the most common cause of pneumonia among patients with AIDS when the CD4 cell counts drop below 200/mm³.

Pathogenesis and Clinical Manifestations

Infectious agents gain access to the lower respiratory tract by the inhalation of aerosolized material, by aspiration of upper airway flora, or by hematogenous seeding. Pneumonia occurs when lung defense mechanisms are diminished or overwhelmed. The major symptoms or pneumonia are cough, chest pain, fever, shortness of breath and sputum production. Patients are tachycardic. Headache, confusion, abdominal pain, nausea, vomiting and diarrhea may be present, depending on the age of the patient and the organisms involved.

Microbiologic Diagnosis

Etiologic diagnosis of pneumonia on clinical grounds alone is almost impossible. Sputum should be examined for a predominant organism in any patient suspected to have a bacterial pneumonia; blood and pleural fluid (if present) should be cultured. A sputum specimen with fewer than 10 while cells per high-power field under a microscope is considered to be contaminated with oral secretions and is unsatisfactory for diagnosis. Acid-fast stains and cultures are used to identify Mycobacterium and Nocardia spp. Most fungal pneumonias are diagnosed on the basis of culture of sputum or lung tissue. Viral infection may be diagnosed by demonstration of antigen in secretions or cultures or by an antibody response. Serologic studies can be used to identify viruses, M pneumoniae, C. burnetii, Chlamydia species, Legionella, Francisella, and Yersinia. A rise in serum cold agglutinins may be associated with M pneumoniae infection, but the test is positive in only about 60% of patients with this pathogen.
Rapid diagnostic tests, as described in previous sections, are available to identify respiratory viruses: the fluorescent-antibody test is used for Legionella. A sputum quellung test can specify S pneumoniae by serotype. Enzyme-linked immunoassay, DNA probe and polymerase chain reaction methods are available for many agents causing respiratory infections.
Some organisms that may colonize the respiratory tract are considered to be pathogens only when they are shown to be invading the parenchyma. Diagnosis of pneumonia due to cytomegalovirus, herpes simplex virus, Aspergillus spp. or Candida spp require specimens obtained by transbronchial or open-lung biopsy. Pneumocystis carinii can be found by silver stain of expectorated sputum. However, if the sputum is negative, deeper specimens from the lower respiratory tract obtained by bronchoscopy or by lung biopsy are needed for confirmatory diagnosis.

Prevention and Treatment

Until the organism causing the infection is identified, decisions on therapy are based upon clinical history, including history of exposure, age, underlying disease and previous therapies, past pneumonias, geographic location, severity of illness, clinical symptoms, and sputum examination. Once a diagnosis is made, therapy is directed at the specific organism responsible.
The pneumococcal vaccine should be given to patients at high risk for developing pneumococcal infections, including asplenic patients, the elderly and any patients immunocompromised through disease or medical therapy. Yearly influenza vaccinations should also be provided for these particular groups. An enteric-coated vaccine prepared from certain serotypes of adenoviruses is available, but is only used in military recruits. In AIDS patients, trimethoprim/sulfamethoxazole, aerosolized pentamidine or other antimicrobials can be given for prophylaxis of Pneumocystis carinii infections.