Walaupun 7 tips pertama anda ikuti, dan anda juga nggak
ngerokok, anda sudah mengurangi kemungkinan serangan jantung sampai dengan 90
persen! Apalagi jika semua anda ikuti.
1. Jalan selama 30 menit setiap hari! Nggak ada alasan!,
lalu setelah itu, coba telepon seseorang. jalan setengah jam setiap hari,
menurunkan resiko serangan jantung sekitar 30 persen. Ini semacam ujian bagi
anda, Jika anda sukses melakukan hal ini, kemungkinan anda mulai akan melakukan
kompromi2 yang lain. Bertelepon dengan orang lain adalah langkah yang sangat
penting: karena akan memperkuat komitmen anda. O yah, coba telepon rekan
perempuan anda, karena mereka akan lebih mendukung anda.
2. Kenali tekanan darah anda, dan lakukan apapun, supaya
mencapai angka 115/75. Tenakan darah anda mungkin bahkan lebih penting daripada
kolesterol anda. Dan, anda bisa menurunkan tekana ini sendiri. Cara terbaik?
Olah raga teratur, dan kurangi lemak di perut. Kenapa? karena lemak ini
menutupi organ2 penting, sehingga, supaya organ2 ini bisa bekerja lebih baik,
dibutuhkan tekanan darah lebih. Jadi, ketika lemak perut berkurang, tekanan
darah yang dibutuhkan akan menurun drastis.
3. Makan 250gr kacang2an setiap hari. Kacang2an akan
meningkatkan kadar kolesterol baik, HDL, dan menurunkan radang. Kacang juga
membantu menyehatkan jantung dengan alasan yang belum jelas. Kacang memiliki
kadar asam lemak Omega 3 tinggi, memiliki protein dan serat tinggi.
4. Coba cari tahu kadar HDL anda dan coba tingkatkan sampai
di nilai 50. Bagi wanita, nilai HDL tinggi jauh lebih baik daripada LDL rendah.
Entah kenapa, tapi yang jelas, makin tinggi nilai HDL, makin bagus (50 sudah
termasuk bagus). CAra termudah untuk meningkatkan nilainya adalah olahraga,
kurangi minuman keras, makan makanan dengan lemak sehat, misalnya: zaitun,
canola. Asam Pantotenat (vit. B5) juga bisa membantu.
5. Makan 10 sendok makan saus tomat dalam seminggu. Ini
adalah tips favorit saya. Saus tomat penuh dengan kalium yang menurunkan
tekanan darah. Yang saya maksud, bukan saus tomat yang asin, gurih dan
berlemak, atau yang disajikan dengan pasta dalam jumlah raksasa. Saus biasa,
sederhana, dan sehat.
6. Secara teratur, gunakan benang gigi. Menghindari penyakit
mulut, mencegah radang arteri, yang membantu anda mengurangi kemungkinan sakit
jantung. Jarang ada orang yang tahu bahwa kesehatan mulut anda mempengaruhi
semua kesehatan arteri anda, yang mempengaruhi keadaan aliran darah ke jantung
dan organ seksual anda, bahkan, mempengaruhi kerutan pada kulit.
7. Jangan makan minyak jenuh lebih dari 20 gram setuap hari,
dan gunakan minyak trans sesedikit mungkin. Lemak jenuh dan lemak trans akan
menyebabkan radang arteri. Cinnamon roll (roti kayu manis) memiliki 7 gram
lemak jenuh. Minyak trans (misalnya dalam mentega atau margarin), sering
ditemukan dalam makanan yang diproses atau dipanggang dalam oven.
8. Baca label, dan segera taruh kembali makanan yang label,
dengan 5 bahan pertama menuliskan gula. Kenapa? urutan bahan diurutkan
berdasarkan kandungan terbanyak. Memang boleh rendah lemak, tapi jika tinggi
gula, sama aja boong. Kenapa? karena jika anda makan gula berlebihan, ujung2nya
jadi lemak juga, yang ditumpuk di sekitar perut.
9. Minum alkohol? kurangi, sehari segelas aja. Kami sendiri
masih belum jelas, tapi minuman beralkohol seperti bir dan anggur memiliki efek
anti – radang. Tapi sering ditemukan bahwa mereka yang tidak minum alkohol sama
sekali, malah memiliki kemungkinan serangan jantung lebih tinggi daripada
mereka yang minum sedikit2. O yah! minum 7 gelas sehari nggak sama efeknya dengna
minum 1 gelas tiap hari!
10. Makan 9 porsi sayuran dan buah setiap hari. Buah dan
sayuran penuh dengan serat. Coba pelan2 tingkatkan jumlahnya dalam 2 – 6
minggu. karena jika jumlahnya meningkat drastis, malah kurang ok hasilnya, dan
mempengaruhi pencernaan anda sendiri!.
The term Proteus signifies
changeability of form, as personified in the Homeric poems in Proteus,
"the old man of the sea," who tends the sealflocks of Poseidon and
has the gift of endless transformation. The first use of the term “Proteus” in
bacteriological nomenclature was made by Hauser (1885) who described under this
term three types of organisms which he isolated from putrefied meat. One of the
three species Hauser identified was Proteus vulgaris so this organism
has a long history in Microbiology.
Over the past two decades the genus Proteus, and in
particular P. vulgaris, has undergone a number of major taxonomic
revisions. In 1982, P. vulgaris was separated into three biogroups on
the basis of indole production. Biogroup one was indole
negative and represented a new species: P. penneri; while biogroup two
and three remained together as P. vulgaris.
Lab Identification
According to laboratory conducted fermentation tests, P.
vulgaris ferments glucose and amygdalin, but does not ferment mannitol or
lactose. P. vulgaris also tests positive for the methyl red (mixed acid
fermentation) test and is also an extremely motile organism.
When P. vulgaris is tested using the API 20E Identification System[1] test strip for enterobacteriaceae (made
by BIOMERIEUX)
[2], it is discovered that it provides a
positive result for: sulfur reduction, urease production, tryptophan deaminase
production, and indole production, and provides a negative result for the
remainder of the tests on the testing strip.
The optimal growing conditions of this organism is in a
facultative anaerobic environment with an average temperature of about 37
degrees Celsius .
The Becton/Dickinson BBL Enterotube II system for
identification of members of the family Enterobacteriaceae inoculated with Proteus
vulgaris may yield the following results: Positive for Glucose fermentation
(with gas production). Negative for Lysine and Ornithine. Positive for Hydrogen
sulfide production and positive for Indole production. Negative for Adonitol
and Lactose. Negative for Arabinose, Sorbitol and Dulcitol. The Phenylalanine
test was positive as was the Harnstoff Urea test. Proteus vulgaris tested positive
for Citrate. All combine for a "Biocode ID of 31407" for use in the
Interpretation Guide/Computer Coding and Identification System (CCIS). Note
that Proteus vulgaris can also test Urease negative in solid media (such as in
Enterotube), but will be Urease positive in liquid media. The CCIS code will
still identify Proteus vulgaris with a negative urease test.
Proteus Infections
Etiology & Epidemiology
Nosocomial
infections
Proteus
mirabilis causes 90% of Proteus infections.
Proteus
vulgaris and Proteus penneri are easily isolated from individuals in
long-term care facilities and hospitals and from patients with underlying
diseases or compromised immune systems.
Patients
with recurrent infections, those with structural abnormalities of the
urinary tract, those who have had urethral instrumentation, and those
whose infections were acquired in the hospital have an increased frequency
of infection caused by Proteus and other organisms (e.g., Klebsiella,
Enterobacter, Pseudomonas, enterococci, staphylococci)
Pathogenesis & Virulence
motilityflagella
adherence factors Fimbriae - facilitate adherence and thus enhance the capacity of the
organism to produce disease
inflammatory response IL-6/IL-8 secretion - attachment to uroepithelial cells initiates
secretion apoptosis and epithelial cell desquamationpyelonephritis
- Bacterial production of urease increases risk bacteremia & sepsis
- bacterial endotoxin (LPS)
Survivalurease
production - alkalinize the urine by hydrolyzing urea to ammonia makes
proteus effective in producing an environment in which it can survive.
Clinical Expression
Bacteremia & sepsis
- Enterobacteriaceae (of which Proteus is a member) and Pseudomonas species are
the microorganisms most commonly responsible for gram-negative bacteremia.
The presence of the sepsis syndrome associated with a UTI
should raise the possibility of urinary tract obstruction. This is especially
true of patients who reside in long-term care facilities, who have long-term
indwelling urethral catheters, or who have a known history of urethral anatomic
abnormalities.
UTI obstruction
- Urease production leads to precipitation of organic and inorganic compounds,
which leads to struvite stone formation. Struvite stones are composed of a
combination of magnesium ammonium phosphate (struvite) and calcium
carbonate-apatite. Struvite stone formation can be sustained only when ammonia
production is increased and the urine pH is elevated to decrease the solubility
of phosphate. Both of these requirements can occur only when urine is infected
with a urease-producing organism such as Proteus. Urease metabolizes urea into
ammonia and carbon dioxide: Urea 2NH3 + CO2. The ammonia/ammonium buffer pair
has a pK of 9.0, resulting in the combination of highly alkaline urine rich in
ammonia.
Symptoms attributable to struvite stones are uncommon. More
often, women present with UTI, flank pain, or hematuria and are found to have a
persistently alkaline urine pH (>7.0).
Treatments
Known antibiotics that P. vulgaris is sensitive to:
Ciprofloxacin
Ceftazidime
Netilmicin
Sulbactam or Cefoperazo
Meropenem
Piperacillin/tazobactam
Unasyn
Antibiotics should be introduced in much higher doses than
"normal" when P. vulgaris has infected the sinus or respiratory
tissues. I.E.- Ciprofloxacin should be introduced at a level of at least
2000 mg per day orally in such a situation, rather than the
"standard" 1000 mg per day.
Sumber : http://en.wikipedia.org/wiki/Proteus_vulgaris
The genus Klebsiella belongs to the tribe
Klebsiellae, a member of the family Enterobacteriaceae. The organisms are named
after Edwin Klebs, a 19th century German microbiologist. Klebsiellae are
nonmotile, rod-shaped, gram-negative bacteria with a prominent polysaccharide
capsule. This capsule encases the entire cell surface, accounts for the large
appearance of the organism on gram stain, and provides resistance against many
host defense mechanisms.
Members of the Klebsiella genus typically express 2
types of antigens on their cell surface. The first is a lipopolysaccharide (O
antigen); the other is a capsular polysaccharide (K antigen). Both of these
antigens contribute to pathogenicity. About 77 K antigens and 9 O antigens
exist. The structural variability of these antigens forms the basis for
classification into various serotypes. The virulence of all serotypes appears
to be similar.
The genus was originally divided into 3 main species based
on biochemical reactions. Today, 7 species with demonstrated similarities in
DNA homology are known. These are (1) Klebsiella pneumoniae, (2) Klebsiella
ozaenae, (3) Klebsiella rhinoscleromatis, (4) Klebsiella oxytoca,
(5) Klebsiella planticola, (6) Klebsiella terrigena, and (7) Klebsiella
ornithinolytica. K pneumoniae is the most medically important
species of the group. K oxytoca and K rhinoscleromatis have also
been demonstrated in human clinical specimens. In recent years, klebsiellae
have become important pathogens in nosocomial infections.[1]
This scanning electron micrograph (SEM) reveals some of the
ultrastructural morphologic features of Klebsiella pneumoniae. Courtesy of
CDC/Janice Carr.
Host defense against bacterial invasion depends on
phagocytosis by polymorphonuclear granulocytes and the bactericidal effect of
serum, mediated in large part by complement proteins. Both classic-pathway and
alternate-pathway complement activation have been described, but the latter,
which does not require the presence of immunoglobulins directed against
bacterial antigens, appears to be the more active pathway in K pneumoniae
infections.
Recent data from preclinical studies suggest a role for
neutrophil myeloperoxidase and lipopolysaccharide-binding protein in host
defense against K pneumoniae infection. Neutrophil myeloperoxidase is thought
to mediate oxidative inactivation of elastase, an enzyme implicated in the
pathogenesis of various tissue-destroying diseases. Lipopolysaccharide-binding
protein facilitates transfer of bacterial cell wall components to inflammatory
cells. Investigators showed higher rates of infection in experimental mice
deficient in the genes that control expression of these 2 agents.
The bacteria overcome innate host immunity through several
means. They possess a polysaccharide capsule, which is the main determinant of
their pathogenicity. The capsule is composed of complex acidic polysaccharides.
Its massive layer protects the bacterium from phagocytosis by polymorphonuclear
granulocytes. In addition, the capsule prevents bacterial death caused by
bactericidal serum factors. This is accomplished mainly by inhibiting the
activation or uptake of complement components, especially C3b. The bacteria
also produce multiple adhesins. These may be fimbrial or nonfimbrial, each with
distinct receptor specificity. These help the microorganism to adhere to host
cells, which is critical to the infectious process.
Lipopolysaccharides (LPS) are another bacterial
pathogenicity factor. They are able to activate complement, which causes
selective deposition of C3b onto LPS molecules at sites distant from the
bacterial cell membrane. This inhibits the formation of the membrane attack
complex (C5b-C9), which prevents membrane damage and bacterial cell death.
Availability of iron increases host susceptibility to K
pneumoniae infection. Bacteria are able to compete effectively for iron
bound to host proteins because of the secretion of high-affinity, low molecular
weight iron chelators known as siderophores. This is necessary because most
host iron is bound to intracellular and extracellular proteins. In order to
deprive bacteria of iron, the host also secretes iron-binding proteins.
Epidemiology
Klebsiellae are ubiquitous in nature. In humans, they may
colonize the skin, pharynx, or gastrointestinal tract. They may also colonize
sterile wounds and urine. Carriage rates vary with different studies.
Klebsiellae may be regarded as normal flora in many parts of the colon and
intestinal tract and in the biliary tract. Oropharyngeal carriage has been
associated with endotracheal intubation, impaired host defenses, and
antimicrobial use.
K pneumoniae
and K oxytoca are the 2 members of this genus responsible for most human
infections. They are opportunistic pathogens found in the environment and in
mammalian mucosal surfaces. The principal pathogenic reservoirs of infection
are the gastrointestinal tract of patients and the hands of hospital personnel.
Organisms can spread rapidly, often leading to nosocomial outbreaks.
Infection with Klebsiella organisms occurs in the
lungs, where they cause destructive changes. Necrosis, inflammation, and
hemorrhage occur within lung tissue, sometimes producing a thick, bloody,
mucoid sputum described as currant jelly sputum. The illness typically affects
middle-aged and older men with debilitating diseases such as alcoholism,
diabetes, or chronic bronchopulmonary disease. This patient population is
believed to have impaired respiratory host defenses. The organisms gain access
after the host aspirates colonizing oropharyngeal microbes into the lower
respiratory tract.
Klebsiellae have also been incriminated in nosocomial
infections. Common sites include the urinary tract, lower respiratory tract,
biliary tract, and surgical wound sites. The spectrum of clinical syndromes
includes pneumonia, bacteremia, thrombophlebitis, urinary tract infection
(UTI), cholecystitis, diarrhea, upper respiratory tract infection, wound
infection, osteomyelitis, and meningitis. The presence of invasive devices,
contamination of respiratory support equipment, use of urinary catheters, and
use of antibiotics are factors that increase the likelihood of nosocomial
infection with Klebsiella species. Sepsis and septic shock may follow
entry of organisms into the blood from a focal source.
Rhinoscleroma and ozena are 2 other infections caused by Klebsiella
species. These diseases are rare. Rhinoscleroma is a chronic inflammatory
process involving the nasopharynx, whereas ozena is a chronic atrophic rhinitis
characterized by necrosis of nasal mucosa and mucopurulent nasal discharge.
K oxytoca
has been implicated in neonatal bacteremia, especially among premature infants
and in neonatal intensive care units. Increasingly, the organism is being
isolated from patients with neonatal septicemia.
Extensive use of broad-spectrum antibiotics in hospitalized
patients has led to both increased carriage of klebsiellae and, subsequently,
the development of multidrug-resistant strains that produce extended-spectrum
beta-lactamase (ESBL). These strains are highly virulent, show capsular type
K55, and have an extraordinary ability to spread. Most outbreaks are due to a
single clone or single gene; the bowel is the major site of colonization with
infection of the urinary tract, respiratory tract, and wounds. Bacteremia and
significant increased mortality have resulted from infection with these
species.
In addition to prior antibiotic use, risk factors for
infection include the presence of an indwelling catheter, feeding tube, or
central venous catheter; poor health status; and treatment in an intensive care
unit or nursing home. Acquisition of these species has become a major problem
in most hospitals because of resistance to multiple antibiotics and potential
transfer of plasmids to other organisms.
In some parts of the world, K pneumoniae is an
important cause of community-acquired pneumonia in elderly persons. Studies
conducted in Malaysia and Japan estimate the incidence rate in elderly persons
to be 15-40%, which is equal to, if not greater than, that of Haemophilus
influenzae. However, in the United States, these figures are different.
Persons with alcoholism are the main population at risk, and they constitute
66% of people affected by this disease. Mortality rates are as high as 50% and
approach 100% in persons with alcoholism and bacteremia.
Klebsiellae are also important in nosocomial infections
among adult and pediatric populations. Klebsiellae account for approximately 8%
of all hospital-acquired infections. In the United States, depending on the
study reviewed, they comprise 3-7% of all nosocomial bacterial infections,
placing them among the top 8 pathogens in hospitals. Klebsiellae cause as many
as 14% of cases of primary bacteremia, second only to Escherichia coli
as a cause of gram-negative sepsis. They may affect any body site, but
respiratory infections and UTIs predominate.
Of 145 reported epidemic outbreaks of nosocomial bacteremias
during 1983-1991, 13 were attributed to Klebsiella organisms. The US
Centers for Disease Control and Prevention report that Klebsiella
strains were responsible for 3% of all pathogenic epidemic outbreaks.
An investigation of Klebsiella pneumoniae
carbapenemase (KPC)-producing Enterobacteriaceae among patients of acute
and long-term acute care hospitals was conducted in 2011. The investigation
found extensive spread of KPC-producing Enterobacteriaceae throughout 4
adjacent counties in Indiana and Illinois over a 1-yr period. Long-term acute
care hospitals played a central role in the outbreak, suggesting that
guidelines for controlling KPC should be expanded to include long-term care facilities.
Education of personnel and coordinated regional efforts among health care
facilities are crucial for KPC control.[2]
K oxytoca
is among the top 4 pathogens that cause infection in patients in neonatal
intensive care units. It is the second most frequent cause of gram-negative
neonatal bacteremia.
International
Outbreaks of neonatal septicemia occur worldwide. Infection
with K pneumoniae also has a worldwide distribution. Infection with K
rhinoscleromatis is not common in the United States, although it has a
worldwide distribution and is usually observed in areas of eastern Europe,
southern Asia, central Africa, and Latin America.
Mortality/Morbidity
Klebsiella pneumonia is a necrotizing process with a predilection
for debilitated people. It has a high mortality rate of approximately 50%
even with antimicrobial therapy. The mortality rate approaches 100% for
persons with alcoholism and bacteremia.
Klebsiella bacteremia and sepsis produce clinical manifestations
similar to those caused by other gram-negative enteric organisms.
Morbidity and mortality rates are comparable to those for other
gram-negative organisms that cause sepsis and septic shock. In neonatal
units, outbreaks caused by ESBL-producing strains present a more serious
problem and may be associated with increased mortality.
Age
Community-acquired
Klebsiella (Friedlãnder) pneumonia is a disease of debilitated
middle-aged and older men with alcoholism.
Nosocomial
infections may affect adults or children, and they occur more frequently
in premature infants, patients in neonatal intensive care units, and
hospitalized individuals who are immunocompromised.
Sumber : http://emedicine.medscape.com/article/219907-overview#showall
Leukemia merupakan bagian dari penyakit kanker, yang mana
masyarakat umum menyebutnya dengan nama Kanker Darah itu karena terjadi pada
sel – sel darah. Leukemia (kanker darah) adalah jenis penyakit yang menyerang
sel – sel darah putih yang diproduksi oleh sumsum tulang (Bone Marrow). Sumsum
tulang atau bone marrow ini dalam tubuh manusia memproduksi tiga tipe sel darah
yang diantaranya adalah sel darah putih ( yang berfungsi sebagai sistem imun /
daya tahan tubuh terhadap infeksi ), sel darah merah ( berfungsi membawa
oksigen kedalam tubuh ) dan platelet (bagian kecil sel darah yang membantu
proses pembekuan darah ).
Leukemia pada umumnya sudah muncul pada diri seseorang sejak usia dini, dimana
sumsum tulang tanpa diketahui dengan jelas penyebabnya telah memproduksi sel
darah putih ayng berkembang tidak normal. Secara normal, sel darah putih
me-reproduksi ulang bila diperlukan oleh tubuh atau ada tempat bagi sel darah
itu sendiri. Tubuh manusia akan memberikan sinyal atau tanda secara teratur
apabila sel darah dibutuhkan untuk be-reproduksi kembali.
Pada kasus Leukemia, sel darah putih ternyata tidak merespon terhadap sinyal
yang diberikan sehingga produksi berlebihan dan tidak terkontrol dan akhirnya
keluar dari sumsum tulang dan dapat ditemukan di dalam darah perifer atau darah
tepi. Seseorang dengan kondisi seperti ini (Leukemia) akan menunjukkan gejala
deperti ini : mudah terkena penyakit infeksi, anemia dan pendarahan.
Leukemia Akut dan Kronis
Leukemia akut ditandai dengan suatu perjalanan penyakit yang sangat cepat,
mematikan dan memburuk. Apabila hal ini tidak segera diobati, maka dapat
menyebabkan kematian dalam hitungan minggu hingga hari. Sedangkan Leukemia
kronis memiliki perjalanan yang tidak begitu cepat sehingga memiliki harapan
hidup yang lebih lama, hingga lebih dari 1 tahun.
Jika berdasarkan sel darah putih yang terkena, baik itu
Limphoid atau Myeloid, maka Leukemia dibagi menjadi : 1. Leukemia Limfositik akut (LLA), merupakan tipe Leukemia paling
sering terjadi pada anak – anak. Tetapi penyakit ini juga terdapat pada dewasa
terutama mereka yang telah berusia 65 tahun atau lebih. 2. Leukemia Mielositik Akut (LMA). Ini lebih sering terjadi pada
dewasa daripada anak – anak. Tipe ini dahullu disebut Leukemia Nonlimfositik
akut. 3. Leukemia Limfositik Kronis (LLK). Orang dewasa yang telah
berusia lebih dari 55 tahun lebih sering terkena Leukemia ini, walaupun orang
dewasa yang masih muda juga bisa terkena ini. Akan tetapi tipe Leukemia ini
hampir tidak pernah terjadi pada anak – anak. 4. Leukemia Mielositik (LMK). Yang ini sering terjadi pada semua
orang dewasa dan dapat juga terjadi pada anak – anak tetapi sangat sedikit.
Penyebab Penyakit Leukemia
Walaupun sampai saat ini belum ada / belum ditemukan penyebab utama dari
Leukemia ini, akan tetapi ada beberapa faktor yang bisa menjadi pemicu
terjadinya Leukemia pada setiap orang, diantaranya adalah : a. Radiasi. Hal ini berdasarkan riset pada pegawai Radiologi yang
ternyata lebih sering menderita Leukemia. Leukemia ini juga ditemukan pada
korban radiasi bom atom di Heroshima dan Nagasaki (Jepang). b. Leukemogenik. Beberapa zat kimia telah diidentifikasi dapat
mempengaruhi frekuensi Leukemia, misalnya racun lingkungan seperti benzena,
bahan kimia industri seperti insektisida serta obat – obatan yang digunakan
untuk kemoterapi. c. Herediter. Yang mana penderita Down Syndrom 20% lebih besar
akan terkena Leukemia daripada orang normal. d. Virus. Ada beberapa jenis virus yang dapat menyebabkan
Leukemia, antara lain : retrovirus, virus leukemia feline, HTLV-1 pada dewasa.
Tanda dan Gejala Penyakit Leukemia
Secara umum tanda dan gejala leukemia dapat digambarkan sebagai berikut; 1. Anemia. Penderita akan merasa cepat lelah, pucat dan bernafas
cepat (dimana sel darah merah di bawah normal sehingga oksigen dalam tubuh
kurang). 2. Pendarahan. Ketika Platelet (sel pembeku darah) tidak
terproduksi secara wajar karena didominasi oleh sel darah putih, sehingga
menyebabkan penderita akan mengalami pendarahan di jaringan kulit (bisa berup
banyaknya jentik merah lebar atau kecil pada jaringan kulit). 3. Terserang Infeksi. Karena sel darah putih tidak bisa berfungsi
secara maksimal sebagai pelindung daya tahan tubuh, sehingga tubuh penderita
mudah terkena virus/bakteri, bahkan dengan sendirinya mengalami demam, keluar
cairan putih dari hidung (meler) dan batuk. 4. Nyeri Tulang dan Persendian. Hal ini disebabkan sebagai akibat
dari sumsum tulang mendesak padat oleh sel darah putih. 5. Nyeri Perut. Nyeri perut juga bisa menjadi indikasai gejala
Leukemia, dimana sel leukemia dapat terkumpul pada organ ginjal, hati dan
empedu yang menyebabkan pembesaran pada organ – organ tubuh dan timbullah
nyeri. 6. Pembengkakan Kelenjar Lympa. Yang bisa terjadi di bawah leher,
lengan dada dan lainnya. Kelenjar Lympa bertugas menyaring darah, karena tidak
berfungsi dengan baik sehingga sel leukemia terkumpul dan mengakibatkan
pembengkakan 7. Kesulitan Bernafas (Dyspnea). Penderita mungkin menampakkan
gejala kesulitan bernafas dan nyeri dada, apabila hal ini terjadi, maka harus
segera mendapatkan pertolongan medis.
Diagnosa Penyakit Leukemia ( Kanker Darah )
Penyakit Leukemia dapat dipastikan dengan beberapa pemeriksaan, diantaranya
adalah : Biopsy, pemeriksaaan darah ( Complete Bloood Count (CBC)), CT atau CAT
scan, Magnetic Resonance Imaging (MRI), X-ray, Ultrasound, Spinal tap/ lumbar
puncture.
Penanganan dan Pengobatan Leukemia
Penanganan kasus Leukemia biasanya berdasarkan gejala – gejala yang muncul
seperti yang telah saya sebutkan diatas. Namun secara garis besar, penanganan
dan pengobatan Leukemia dapat dilakukan dengan cara single atau gabungan dari
beberapa metode dibawah ini : a. Chemotherapy / intrathecal medications.
b. Therapy Radiasi (metode ini sangat jarang dilakuikan).
c. Transplantasi bone marrow (sumsum tulang).
d. Pemberian obat – obatan tablet dan suntik.
5. Transfusi sel darah merah atau Platelet.
Sedangkan sistem therapi yang sering digunakan adalah kombinasi antara Chemotherapy
dan pemberian obat – obatan yang berfokus pada pemberhentian produksi sel darah
putih yang tidak normal dalam bone marrow. Selanjutnya adalah penanganan
terhadap beberapa gejala dan tanda – tanda yang telah ditampakkan oleh tubuh
penderita dengan monitor yang komprehensive. Dan bagi yang membutuhkan file
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Fleas are the insects forming the orderSiphonaptera. They are wingless, with mouthparts adapted for piercing
skin and sucking blood. Fleas are external parasites, living by hematophagy off the blood
of mammals (including bats and humans) and birds.
Fleas are wingless insects (1/16 to 1/8-inch (1.5 to
3.3 mm) long) that are agile, usually dark colored (for example, the
reddish-brown of the cat flea), with tube-like mouth-parts adapted to feeding
on the blood of their hosts. Their legs are long, the hind pair well adapted for
jumping: a flea can jump vertically up to 7 inches (18 cm) and
horizontally up to 13 inches (33 cm).[3] This is around 1200 to 2200 times
their own body length, making the flea one of the best jumpers of all known
animals (relative to body size), second only to the froghopper. According to an article in Science
News, "researchers with the University of Cambridge in England have
shown that fleas take off from their tibiae and tarsi—the insect equivalent of
feet—and not their trochantera, or knees. The researchers report their
conclusion in the March 1 Journal of Experimental Biology."[4]
It has been known that fleas do not use muscle power but energy stored in a
protein named resilin but the researchers used high-speed
video technology and mathematical models to discover where the spring action
actually happens. Their bodies are laterally compressed, permitting easy
movement through the hairs or feathers on the host's body (or in the case of
humans, under clothing). The flea body is hard, polished, and covered with many
hairs and short spines directed backward,[5] which also assist its movements
on the host. The tough body is able to withstand great pressure, likely an
adaptation to survive attempts to eliminate them by mashing or scratching. Even
hard squeezing between the fingers is normally insufficient to kill a flea. It
is possible to eliminate them by pressing individual fleas with adhesive tape
or softened beeswax (or "cheese" wax) or by rolling a flea briskly
between the fingers to disable it then crushing it between the fingernails.
Fleas also can be drowned in water and may not survive direct contact with
anti-flea pesticides
Fleas lay tiny white oval-shaped eggs better viewed through
a loupe. The larva is small, pale, has
bristles covering its worm-like body, lacks eyes, and has mouthparts adapted to
chewing. The larvae feed on various organic matter, especially the feces of
mature fleas. The adult flea's diet consists solely of fresh blood.[6] In the pupal phase, the larva is
enclosed in a silken, debris-covered cocoon.
Life cycle and habitat
Fleas are holometabolous insects, going through the
four life cycle
stages of egg, larva,
pupa,
and imago (adult). The flea life cycle begins
when the female lays after feeding. Adult fleas must feed on blood before they
can become capable of reproduction.[5] Although reproduction is normally
asexual, for at least one specie, under stress conditions, female fleas produce
male fleas. [7]. Eggs are laid in batches of up
to 20 or so, usually on the host itself, which means that the eggs can easily
roll onto the ground. Because of this, areas where the host rests and sleeps
become one of the primary habitats of eggs and
developing fleas. The eggs take around two days to two weeks to hatch.[3]
Flea larvae emerge from the eggs to feed on any available
organic material such as dead insects, feces, and vegetable matter. They are
blind and avoid sunlight, keeping to dark places like sand, cracks and
crevices, and bedding. Given an adequate supply of food, larvae should pupate and weave a silken
cocoon within 1–2 weeks after 3 larval stages. After another week or two, the
adult flea is fully developed and ready to emerge from the cocoon. They may
however remain resting during this period until they receive a signal that a
host is near - vibrations (including sound), heat, and carbon dioxide are all stimuli indicating
the probable presence of a host.[3] Fleas are known to overwinter in the larval or pupal stages.
Once the flea reaches adulthood, its primary goal is to find
blood and then to reproduce.[8]
Adult fleas only have about a week to find food once they emerge, but after
that they can survive two months to a year between meals. Flea populations are
unevenly distributed, with about 50% eggs, 35% larvae, 10% pupae, and 5%
adults.[3] Their total life cycle can be as
short as two weeks, but may be several months in ideal conditions. Female fleas
can lay 500 or more eggs over their life, allowing for phenomenal growth rates.
Adult female rabbit fleas, Spilopsyllus cuniculi, can
detect the changing levels of cortisol and corticosterone, hormones in the
rabbit's blood that indicate she is getting close to giving birth. This
triggers sexual maturity in the fleas and they start producing eggs. As soon as
the baby rabbits are born, the fleas make their way down to them and once on
board they start feeding, mating, and laying eggs. After 12 days, the adult
fleas make their way back to the mother. They complete this mini-migration
every time she gives birth.[9]
Newly emerged adult fleas live only about one week if a
blood meal is not obtained. However, completely developed adult fleas can live
for several months without eating, so long as they do not emerge from their
puparia. Optimum temperatures for the flea's life cycle are 70°F to 85°F (21°C
to 30°C) and optimum humidity is 70%.[9]
Classification
Cat
flea
Fleas are related to mecoptera,[10] winged insects with good
eyesight. The flightless boreid
(snow scorpionfly) with its rudimentary wings
seems to be close to the common ancestor of the 2000 or so known varieties of
flea, which split off in many directions around 160 million years ago.[10] Their evolution continued to
produce adaptations for their specialized parasitic niche, such that they now
have no wings and their eyes are covered over. The large number of flea species
may be attributed to the wide variety of host species they feed on, which
provides so many specific ecological niches to adapt to.
In the past, it was most commonly supposed that fleas had
evolved from the flies (Diptera),
based on similarities of the larvae. (Some authorities use the name Aphaniptera
because it is older, but names above
family rank need not follow the ICZN
rules of priority, so most taxonomists use the
more familiar name). Genetic and
morphological evidence indicates that they are descendants of the Scorpionfly family Boreidae, which are also flightless;
accordingly it is possible that they will eventually be reclassified as a
suborder within the Mecoptera. In any case,
all these groups seem to represent a clade
of closely related insect lineages, for which the names Mecopteroidea and
Antliophora have been proposed.
Flea systematics are not
entirely fixed. While, compared to many other insect groups, fleas have been
studied and classified fairly thoroughly, details still remain to be learned
about the evolutionary relationships among the
different flea lineages.
Fleas are a nuisance to their hosts, causing an itching
sensation which in turn may result in the host attempting to remove the pest by
biting, pecking, scratching, etc. in the vicinity of the parasite. Fleas are
not simply a source of annoyance, however. Some people and animals suffer allergic reactions to flea saliva resulting in rashes.
Flea bites generally result in the formation of a slightly raised, swollen
itching spot with a single puncture point at the center (similar to a mosquito bite). The bites often appear in
clusters or lines of two bites, and can remain itchy and inflamed for up to
several weeks afterwards. Fleas can also lead to hair loss as a result of
frequent scratching and biting by the animal, and can cause anemia in extreme cases.[11]:126
As a vector
Besides the problems posed by the creature itself, fleas can
also act as a vector
for disease. Fleas transmit not only a variety
of viral, bacterial and rickettsial diseases to humans and other
animals, but also protozoans and helminths.[12]:72–73
protozoa:
Trypanosome protozoans such as those
of the subgenusHerpetosoma,
use a variety of flea species opportunistically as vectors.[12]:74
Fleas that specialize as parasites on specific mammals may
use other mammals as hosts; therefore humans are susceptible to the predation
of more than one species of flea.[15]
A misconception concerning the carrying/transmission of the
HIV/AIDS by fleas has been debunked by the Centers for Disease Control and
Prevention (CDC 2003), which stated that fleas cannot carry the virus and
spread it to other humans.
Flea
and tick repellant powder being applied to a dog
Modern flea control is approached using Integrated
Pest Management (IPM) protocols at the host (pet) level. IPM is
achieved by targeting fleas during at least two separate life stages, with at
least two separate molecules. This is typically achieved using an adulticide to kill adult fleas and an
insect development inhibitor (IDI), like lufenuron, or insect growth regulator
(IGR), like methoprene, to prevent development of
immature stages. Flea adults, larvae, or eggs can be controlled with insecticides. Lufenuron is a veterinary preparation
(Program) that attacks the larval flea's ability to produce chitin but does not kill fleas. Flea medicines need to
be used with care because many of them also affect mammals.
Cedar oil, a
non-toxic natural substance, has been proven effective in the eradication of
infestations in pets. Cedar oil is being used to treat sand-flea infestation of
US Military forces in the Persian Gulf.[18]
Since more than three quarters of a flea's life is spent
somewhere other than on the host animal, it is not adequate to treat only the
host; it is important also to treat the host's environment. Thorough vacuuming,
washing linens in hot water, and treating all hosts in the immediate
environment (the entire household, for example) are essential and if possible
on a regular basis.[19]
Contemporary commercial products for the topical treatment
of flea infestations on pets contain pesticides such as imidacloprid, permethrin, and (S)-methoprene. All flea control products are
recommended to be used at least half-yearly because the lifecycle
of flea and tick can last to up to 6 months, and by using one of the flea and
tick control products for so long, the infestation is highly prevented and, in
the end, stopped. Although all these products are effective in fighting against
flea and tick infestations, they have different active
ingredients and, because cats cannot metabolize some of the compounds of the
product, care must be taken in their use.
For the home
Combatting a flea infestation in the home takes patience
because for every flea found on an animal, there could be many more developing
in the home. A spot-on insecticide will kill the fleas on the pet and in turn
the pet itself will be a roving flea trap and mop up newly hatched fleas. The
environment should be treated with a fogger or spray insecticide containing an insect growth regulator, such as pyriproxyfen or methoprene to kill eggs and pupae, which
are quite resistant against insecticides. Frequent vacuuming is also helpful,
but the vacuum bag must be disposed of immediately afterwards. Fleas tend to
breed exponentially in piles of shoes.
Flea
"dirt" in the fur of a cat is actually excess blood from the host
consumed by the adult flea and passed as feces
Diatomaceous earth
can also be used as a home flea treatment in lieu of acetylcholinesterase
inhibitory treatments or insecticides which carry with them a risk of poisoning
for both humans and animals. However, diatomaceous earth is at least
potentially dangerous to pets and people when inhaled, so care in use is
recommended.
Dried pennyroyal has been
suggested as a natural flea control,[20]
but is not recommended in homes with pets due to its high toxicity to mammals.[21]
Borax is sold as a "Natural Laundry
Booster" and can also be used as another home treatment for flea
infestations. Borax contains sodium borate which kills
fleas by dehydrating them, but its safety for pets is untested.[22]
Using dehumidifiers with
air
conditioning and vacuuming all may interrupt the flea life cycle.
Humidity is critical to flea survival. Eggs need relative humidity of at least
70–75% to hatch, and larvae need at least 50% humidity to survive. In humid
areas, about 20% of the eggs survive to adulthood; in arid
areas, less than 5% complete the cycle.[23] Fleas thrive at higher
temperatures, but need 70° to 90°F (21° to 32°C) to survive. Lower temperatures
slow down or completely interrupt the flea life-cycle. A laboratory study done
at the University of
California showed that vacuuming catches about 96% of adult fleas. A
combination of controlled humidity, temperature, and vacuuming should eliminate
fleas from an environment. Altering even one of these environmental factors may
be enough to drastically lower and eliminate an infestation.
