riocaesar : Tipes atau Tipus? Manakah Kata yang Benar?

Sebenarnya banyak sekali para dokter dan tenaga kesehatan lainnya yang tidak menghiraukan penggunaan kata tipes ataupun tipus
sehingga kata-kata ini lazim sekali digunakan oleh masyarakat untuk mendeskripsikan penyakit yang disebabkan oleh infeksi dari
Salmonella typhi ini.

Kuman Salmonella typhi penyebab demam tifoid

Kata yang seharusnya dipakai adalah Demam Tifoid diambil dari kata bahasa Inggris yaitu Typhoid Fever. Tyhphoid pun diambil dari kata
Typhus dan oid yang artinya palsu atau menyerupai, jadi sebenarnya penyakit yang disebabkan oleh S. typhi ibu bukanlah penyakit typhus
yang sebenarnya, melainkan menimbulkan gejala yang serupa dengan penyakit Typhus yang sebenarnya disebabkan oleh parasit
Rickettsia, yang hampir tidak ditemukan di Indonesia.

Epidemic typhus

Berbeda dengan typhus, demam tifoid ini disebabkan oleh kuman S. typhi yang penyebarannya bukan melalui gigitan kutu yang membawa
parasit Rickettsia di dalam tubuhnya, melainkan melalui minuman serta makanan yang terkontaminasi oleh kotoran manusia yang
mengandung kuman tersebut, sehingga bisa dikatakan penyakit ini ditularkan melalui mengonsumsi makanan yang tercemar.

Adapun transmisi dari kuman ini tidak hanya melalui jari manusia yang terkontaminasi kuman ataupun air atau makanan yang sanitasinya
buruk, dapat juga melalui lalat yang menempel dari kotoran manusia ke makanan yang siap dimakan oleh manusia.

Jadi para pembaca setia, sebagai sosialisasi penulis menganjurkan mulai dari sekarang untuk lebih berkenan menggunakan kata "demam
tifoid" dibandingkan kata "types" ataupun "tipes" maupun "tipus" karena memang kata tersebut sama sekali menggambarkan penyakit
yang berbeda dengan yang sebenarnya.

Sumber :
1. http://www.nlm.nih.gov/medlineplus/ency/article/001332.htm
2. http://www.cdc.gov/ncidod/dbmd/diseaseinfo/TyphoidFever_g.htm
3. http://www.cdc.gov/nczved/divisions/dfbmd/diseases/typhoidfever_g
Background
Typhus refers to a group of infectious diseases that are caused by rickettsial organisms and that result in an acute febrile illness. Arthropod
vectors transmit the etiologic agents to humans. The principle diseases of this group are epidemic or louse-borne typhus and its
recrudescent form known as Brill-Zinsser disease, murine typhus, and scrub typhus. (For more information on pediatric scrub typhus, see
the eMedicine article Scrub Typhus in the Pediatric: General Medicine volume.)
Pathophysiology
Epidemic typhus is the prototypical infection of the typhus group of diseases, and the pathophysiology of this illness is representative of
the entire category. The arthropod vector of epidemic typhus is the body louse (Pediculus corporis). This is the only vector of the typhus
group in which humans are the usual host. Rickettsia prowazekii, which is the etiologic agent of typhus, lives in the alimentary tract of the
louse. A Rickettsia- harboring louse bites a human to engage in a blood meal and causes a pruritic reaction on the host's skin. The louse
defecates as it eats; when the host scratches the site, the lice are crushed, and the Rickettsia- laden excrement is inoculated into the bite
wound. The Rickettsia travel to the bloodstream and rickettsemia develops.
Rickettsia parasitize the endothelial cells of the small venous, arterial, and capillary vessels. The organisms proliferate and cause
endothelial cellular enlargement with resultant multiorgan vasculitis. This process may cause thrombosis, and the deposition of
leukocytes, macrophages, and platelets may result in small nodules. Thrombosis of supplying blood vessels may cause gangrene of the
distal portions of the extremities, nose, ear lobes, and genitalia. This vasculitic process may also result in loss of intravascular colloid with
subsequent hypovolemia and decreased tissue perfusion and, possibly, organ failure. Loss of electrolytes is common.
Some people with a history of typhus may develop a recrudescent type of typhus known as Brill-Zinsser disease. After a patient with
typhus is treated with antibiotics and the disease appears to be cured, Rickettsia may linger in the body tissues. Months, years, or even
decades after treatment, organisms may reemerge and cause a recurrence of typhus. How the Rickettsia organisms linger silently in a
person and by what mechanism recrudescence is mediated are unknown. The presentation of Brill-Zinsser disease is less severe than
epidemic typhus, and the associated mortality rate is much lower. Risk factors that may predispose to recrudescent typhus include
improper or incomplete antibiotic therapy and malnutrition.
Murine typhus and scrub typhus share the same pathophysiology as epidemic typhus, although they are somewhat milder. The incubation
period is approximately 12 days for the typhus group. Prior infection with Rickettsia typhi provides subsequent and long-lasting immunity
to reinfection.
Epidemiology
Frequency
United States
Approximately 15 documented sporadic cases of active infection with R prowazekii, the etiologic agent of epidemic typhus, have been
reported. These occurred in the central and eastern portions of the United States and have been linked with exposure to flying squirrels
(Glaucomys volans).[1] The flying squirrel acts as the host for R prowazekii, and transmission to humans is believed to occur via squirrel
fleas or lice. Murine typhus caused by infection with Rickettsia felis is associated with opossums,[2] cats, and their fleas and occurs in
southern California and southern Texas. Most cases of murine typhus in Texas occur in spring and summer, whereas, in California, the
illness is most common in the summer and fall. Murine typhus is most common in adults, but infection may occur in any age group.[3] No
indigenous cases of scrub typhus have occurred in the United States, although infections have been diagnosed in patients returning from
endemic areas.
International
Epidemic typhus occurs in Central and South America, Africa, northern China, and certain regions of the Himalayas. Outbreaks may occur
when conditions arise that favor the propagation and transmission of lice. Brill-Zinsser disease develops in approximately 15% of people
with a history of primary epidemic typhus.
Murine typhus occurs in most parts of the world, particularly in subtropical and temperate coastal regions. Murine typhus occurs mainly in
sporadic cases, and incidence is probably greatly underestimated in the more endemic regions. Rats, mice, and cats, which are hosts for
the disease, are particularly common along coastal port regions. Populations of the flea vector may rise during the summer months in
temperate climates, subsequently increasing the incidence of murine typhus. The homeless are particularly vulnerable.[4] Prior infection
with R typhi provides immunity to subsequent reinfection.
Scrub typhus occurs in the western Pacific region, northern Australia, and the Indian subcontinent. The incidence of scrub typhus is largely
unknown. Many cases are undiagnosed because of its nonspecific manifestations and the lack of laboratory diagnostic testing in endemic
areas. However, one study found that the incidence of scrub typhus in Malaysia was approximately 3% per month, and multiple infections
in the same individual are possible because of a lack of cross-immunity among the various strains of its causative organism, Orientia
tsutsugamushi.[5]
Mortality/Morbidity
Epidemic typhus causes the most severe clinical presentation among the typhus group of rickettsial infections. Patients with severe
epidemic typhus may develop gangrene, leading to a loss of digits, limbs, or other appendages. The vasculitic of epidemic typhus process
may also lead to CNS dysfunction, ranging from dullness of mentation to coma, multiorgan system failure, and death. Untreated epidemic
typhus carries a mortality rate of as low as 20% in otherwise healthy individuals and as high as 60% in elderly or debilitated persons. Since
the advent of widely available antibiotic treatment, the mortality rates associated with epidemic typhus have fallen to approximately 3-
4%. The mortality rate among treated patients with murine typhus is 1-4% and less than 1% for scrub typhus.
Sex
The typhus group of infections has no sexual predilection.
Age
The typhus group of infections has no age predilection. However, in the United States, murine typhus and sporadic cases of epidemic
typhus have mainly occurred in adults.
History
Patients with typhus may have a history that includes the following:
Patients may have had exposure to an endemic area
Occupational exposure: Medical and military personnel are potentially at higher risk for typhus than the general population in endemic
areas.
Overcrowding leads to close personal contact and spread of arthropod vectors (particularly lice) among individuals.
Lack of personal hygiene: Infrequent bathing and changing of clothes provides a hospitable environment for body lice.
Appropriate season: Cold weather may lead to overcrowding indoors and infrequent bathing and changing of clothes, which are
advantageous for lice. Flea vectors are more abundant in warmer weather, when their hosts are more plentiful.
Abrupt onset of fever, headache, and rash are common symptoms in rickettsial infections.
Patients may have a history of flea bite.
History may include exposure to natural disaster or war.
Other less common symptoms of typhus include nonproductive cough and deafness/tinnitus.
The duration of most clinical symptoms and signs in untreated typhus is approximately 2 weeks. Several months may pass before
complete recovery from fatigue and malaise.
Epidemic typhus is the prototypical infection of the typhus group. As described in the Pathophysiology section, typhus is a multisystem
vasculitis and may cause a wide array of clinical manifestations.
Fever is characterized by abrupt onset.
Headache is characterized by abrupt onset and is unremitting.
A maculopapular/petechial rash occurs on days 4-7 and may begin on the axilla and trunk and spread peripherally. The rash of Rocky
Mountain spotted fever (RMSF) typically begins on the extremities and spreads centrally.
Other symptoms of typhus may include rigors, myalgias, malaise, and CNS symptoms (ranging from mental dullness to coma).
Scrub typhus may be difficult to recognize and diagnose because the symptoms and signs of the illness are often nonspecific.
A painless papule develops at the site of the chigger bite and subsequently undergoes central necrosis with formation of an eschar.
Regional lymphadenopathy, with development of large and tender lymph nodes, occurs at the site of the bite and may lead to generalized
lymphadenopathy.
The nonspecific presentation and lack of the characteristic eschar in 40% of patients leads to many undiagnosed cases of scrub typhus.
Physical
Fever
Fever rises to 39-41ºC and is persistent in patients with untreated typhus.
Patients with typhus have relative bradycardia with the fever.
Fever may persist for 24-72 hours after initiation of antibiotic therapy.
Tachypnea and cough: This is most common in scrub typhus because of frequent pulmonary involvement.
Rash
The macular, maculopapular, or petechial rash initially occurs on the trunk and axilla and spreads to involve the rest of the body except for
the face, palms, and soles.
Rash may be petechial in patients with epidemic or murine typhus.
Regional lymphadenopathy
This occurs in scrub typhus in the region of the arthropod bite and inoculation. Generalized lymphadenopathy may follow.
Lymph nodes are often tender and enlarged.
Generalized lymphadenopathy
Eschar
This is found in the scrub form of typhus and is essential in confirming a clinical diagnosis. It occurs in up to 60% of cases.
Eschar occurs at the site of the arthropod bite. It starts as a painless papule, and the lesion becomes indurated and enlarged. The center of
the lesion becomes necrotic and develops into a black scab.
Other features
Mild splenomegaly may occur.
Mild hepatomegaly may occur.
Conjunctival suffusion may occur in scrub typhus.
Causes
Typhus is an acute febrile illness caused by rickettsial organisms. Rickettsia are pleomorphic bacteria that may appear as cocci or bacilli
and are obligate intracellular parasites.
Epidemic typhus is caused by the bacterium R prowazekii, and the vector is the body louse.
P corporis is the most common louse vector; however, Pediculus capitis and Phthirus pubis also transmit epidemic typhus.
Humans are the host in epidemic typhus, but the flying squirrel has also been linked with the disease in several cases in the United
States.[1]
The louse becomes infected with R prowazekii after feeding on a rickettsemic person with a primary case of typhus or during a
recrudescent case (Brill-Zinsser disease).
Of all the typhus vectors, the louse is the only arthropod that dies of this infection. Rickettsia live in the alimentary tract and cause
obstruction and subsequent death of the louse after 2-3 weeks of infection.
All arthropod vectors cause inoculation of Rickettsia into the host by the same mechanism described above (see Pathophysiology).
Murine typhus is caused by R typhi, and the vector is the rat or cat flea (Xenopsylla cheopis, Ctenocephalides felis).
Rats (Rattus rattus), mice, and cats are the usual hosts; human infection is accidental.
Fleas become infected after engaging in a blood meal of a rickettsemic host; however, the fleas are not affected by the bacteria as are the
lice in epidemic typhus.
Infected fleas may subsequently cause disease by direct inoculation or by indirect inoculation of the infected feces into the site of the bite
wound.
Aerosolization of the feces and inoculation into the respiratory tract or into a mucous membrane are other possible routes of infection.
Scrub typhus is caused by O tsutsugamushi (formerly Rickettsia tsutsugamushi) via the mite Leptotrombidium akamushi and possibly
Leptotrombidium deliense.
The life cycle of the mite involves 4 stages of development, but only the larval stage (chigger) requires a blood meal and is infectious to
humans and other mammals.
Once the mite is infected, it acts as a reservoir for Rickettsia.
The infection is maintained in mites from generation to generation by transovarial transmission.
Humans are accidental hosts in scrub typhus; rats, mice, and larger mammals are the usual hosts.