Infeksi Protozoa dan Mikosis Dalam 2014 – dr.

Ruben Dharmawan
Malaria
Essentials of diagnosis
1. Residence or exposure in a malaria-endemic area.
2. Intermittent attacks of chills, fever, and sweating.
3. Headache, myalgia, vomiting, splenomegaly; anemia, thrombocytopenia.
4. Intraerythrocytic parasites identified in thick or thin blood smears.
5. Complications of falciparum malaria: cerebral malaria, severe anemia, hypotension, noncardiogenic
pulmonary edema, acute kidney injury, hypoglycemia, acidosis, and hemolysis.

General Considerations
Malaria is the most important parasitic disease of humans, causing hundreds of millions of
illnesses and nearly a million deaths each year. The disease is endemic in most of the tropics, including
much of South and Central America, Africa, the Middle East, the Indian subcontinent, Southeast Asia,
and Oceania. Transmission, morbidity, and mortality are greatest in Africa, where most deaths from
malaria are in young children. Malaria is also common in travelers from non-endemic areas to the
tropics. Four species of the genus Plasmodium classically cause human malaria. Plasmodium
falciparum is responsible for nearly all severe disease. It is endemic in most malarious areas and is by
far the predominant species in Africa. Plasmodium vivax is about as common as P falciparum, except
in Africa. P vivax uncommonly causes severe disease, although this outcome may be more common
than previously appreciated. Plasmodium ovale and Plasmodium malariae are much less common
causes of disease, and generally do not cause severe illness. Plasmodium knowlesi, a parasite of
macaque monkeys, is now recognized to cause occasional illnesses, including some severe disease, in
humans in Southeast Asia. Malaria is transmitted by the bite of infected female anopheline mosquitoes.
During feeding, mosquitoes inject sporozoites, which circulate to the liver, and rapidly infect
hepatocytes, causing asymptomatic liver infection. Merozoites are subsequently released from the
liver, and they rapidly infect erythrocytes to begin the asexual erythrocytic stage of infection that is
responsible for human disease. Multiple rounds of erythrocytic development, with production of
merozoites that invade additional erythrocytes, lead to large numbers of circulating parasites and
clinical illness. Some erythrocytic parasites also develop into sexual gametocytes, which are infectious
to mosquitoes, allowing completion of the life cycle and infection of others. Malaria may uncommonly
be transmitted from mother-to-infant (congenital malaria), by blood transfusion, and in non-endemic
areas by mosquitoes infected after biting infected immigrants or travelers. In P vivax and P ovale,
parasites also form dormant liver hypnozoites, which are not killed by most drugs, allowing subsequent
relapses of illness after initial elimination of erythrocytic infections. For all plasmodial species,
parasites may recrudesce following initial clinical improvement after suboptimal therapy. In highly
endemic regions, where people are infected repeatedly, antimalarial immunity prevents severe disease
in most older children and adults. However, young children, who are relatively non-immune, are at
high risk for severe disease from P falciparum infection, and this population is responsible for most
deaths from malaria. Pregnant women are also at increased risk for severe falciparum malaria. In areas
with lower endemicity, individuals of all ages commonly present with uncomplicated or severe
malaria. Travelers, who are generally non-immune, are at high risk for severe disease from falciparum
malaria at any age.

Clinical Findings
A. Symptoms and Signs
An acute attack of malaria typically begins with a prodrome of headache and fatigue, followed
by fever. A classic malarial paroxysm includes chills, high fever, and then sweats. Patients may appear
to be remarkably well between febrile episodes. Fevers are usually irregular, especially early in the
illness, but without therapy may become regular, with 48-hour cycles (P vivax and P ovale) or 72-hour
cycles (P malariae), especially with non-falciparum disease. Headache, malaise, myalgias, arthralgias,
cough, chest pain, abdominal pain, anorexia, nausea, vomiting, and diarrhea are common. Seizures
may represent simple febrile convulsions or evidence of severe neurologic disease. Physical findings
may be absent or include signs of anemia, jaundice, splenomegaly, and mild hepatomegaly. Rash and
lymphadenopathy are not typical in malaria, and thus suggestive of another cause of fever. In the
developed world, it is imperative that all persons with suggestive symptoms, in particular fever, who
have traveled in an endemic area be evaluated for malaria. The risk for falciparum malaria is greatest
within 2 months of return from travel; other species may cause disease many months—and
occasionally more than a year—after return from an endemic area.

Severe malaria is defined as the presence of signs of severe illness or organ dysfunction or a
high parasite load (peripheral parasitemia >5% or >200,000 parasites/mcL). It is principally a result of
P falciparum infection because this species uniquely infects erythrocytes of all ages and mediates the
sequestration of infected erythrocytes in small blood vessels, thereby evading clearance of infected
erythrocytes by the spleen. Severe falciparum malaria can include dysfunction of any organ system,
including neurologic abnormalities progressing to alterations in consciousness, repeated seizures, and
coma (cerebral malaria); severe anemia; hypotension and shock; non-cardiogenic pulmonary edema
and the acute respiratory distress syndrome; acute kidney injury due to acute tubular necrosis or, less
commonly, severe hemolysis; hypoglycemia; acidosis; hemolysis with jaundice; hepatic dysfunction;
retinal hemorrhages and other fundoscopic abnormalities; bleeding abnormalities, including
disseminated intravascular coagulation; and secondary bacterial infections, including pneumonia and
Salmonella bacteremia. In the developing world, severe malaria and deaths from the disease are mostly
in young children, in particular from cerebral malaria and severe anemia. Cerebral malaria is a
consequence of a single severe infection while severe anemia follows multiple malarial infections,
intestinal helminths, and nutritional deficiencies. Uncommon disorders resulting from immunologic
responses to chronic infection are massive splenomegaly and, with P malariae infection, immune
complex glomerulopathy with nephrotic syndrome. HIV-infected individuals are at increased risk for
malaria and for severe disease, in particular with advanced immunodeficiency.

CLINICAL PICTURE AND OUTCOME of P. knowlesi.

The clinical picture and outcome of P. knowlesi infection is described in a prospective study
involving 107 patients in the-Sarawak hospital in Malaysia during the period 2006–2008 [15]. The
clinical and laboratory profiles of these patients resembled those of patients infected with other
Plasmodium species. A Vietnamese report suggests that asymptomatic infections may also occur [34].
In Malaysia, the patients with P. knowlesi infection typically presented with a nonspecific febrile
illness with daily fever and chills. Other frequent symptoms included headache, rigors, malaise,
myalgia, abdominal pain, breathlessness, and productive cough. Tachypnea, pyrexia, and tachycardia
were common clinical signs. All patients had thrombocytopenia at hospital admission or on the
following day, yet none of the patients had clinical coagulopathy. At hospital admission, only a few of
the patients had anemia, whereas mild hepatic dysfunction was relatively common. The great majority
of patients (94%) experienced no complications, and the infection responded well to chloroquine and
primaquine treatment [15]. Applying the World Health Organization criteria for P. falciparum
infection, P. knowlesi infection was evaluated as severe in 7% of the cases, with the most frequent
complication being respiratory distress with pulmonary rather than metabolic etiology. A strong
correlation was found between parasite density and the development of respiratory distress. Parasite
density was also strongly and independently associated with renal dysfunction. Two of the patients
died, representing a case fatality rate of 1.8% [15]. Phylogenically, P. knowlesi is relatively closely
related with P. vivax; therefore, it is not surprising that infections with these 2 species share some
common features, such as occasional severity and marked thrombocytopenia [35]. However, disease
caused by P. knowlesi is somewhat more severe than disease caused by P. vivax, although also vivax
malaria can be severe in a significant number of cases, at least in certain regions (severe malaria in
_3%, compared with 7% in individuals with P. knowlesi malaria) [15, 35]. In P. knowlesi infections,
neurological symptoms are rare, and no cases of cerebral malaria have been reported [15]. A post-
mortem study of a lethal P. knowlesi case suggests, however, that P. knowlesi–infected red cells can
sequester in capillaries of the brain, heart, and kidneys [16]. Similarly to P. falciparum, P. knowlesi
can cause severe or even fatal disease. It has a short lifecycle of 24 h [1], enabling a rapid progression
of the disease (Table 1). The erythrocyte invasion by P. knowlesi is not restricted to young or old cells,
which allows high parasitemia, and development of the parasite in erythrocytes is asynchronous. The
threshold for hyperparasitemia in P. knowlesi infections is lower than in P. falciparum malaria and, at
least theoretically, hyperparasitemia, together with the shorter asexual cycling time, may even render
P. knowlesi more virulent in its severe form. In 3 of the 5 reported lethal cases, a high parasitemia was
seen (15%,.10%, and .10 parasites per high-power microscope field) [13, 16]. Clinicians treating these
patients should be aware of the potential lethal outcome of the infection.
Toxoplasmosis
Essentials of diagnosis
1. Infection confirmed by isolation of Toxoplasma gondii or identification of tachyzoites in tissue or
body fluids.
2. Primary infection
`` Fever, malaise, headache, sore throat.
`` Lymphadenopathy.
`` Positive IgG and IgM serologic tests.
3. Congenital infection
`` Follows acute infection of seronegative mothers and leads to CNS abnormalities and
retinochoroiditis.
4. Infection in immunocompromised persons
`` Reactivation leads to encephalitis, retinochoroiditis, pneumonitis, myocarditis.
`` Positive IgG but negative IgM serologic tests.

General Considerations
T gondii, an obligate intracellular protozoan, is found worldwide in humans and in many species of
mammals and birds. The definitive hosts are cats. Humans are infected after ingestion of cysts in raw
or undercooked meat, ingestion of oocysts in food or water contaminated by cats, transplacental
transmission of trophozoites or, rarely, direct inoculation of trophozoites via blood transfusion or organ
transplantation. Toxoplasma seroprevalence varies widely. It has decreased in the United States to
about 20–30%, but it is much higher in other countries in both the developed and developing worlds,
where it may exceed 80%.

Clinical Findings
A. Symptoms and Signs
The clinical manifestations of toxoplasmosis may be grouped into four syndromes.
1. Primary infection in the immunocompetent person—
After ingestion, T gondii infection progresses from the gastrointestinal tract to lymphatics, and then
dissemination. Most acute infections are asymptomatic. About 10–20% are symptomatic after an
incubation period of 1–2 weeks. Acute infections in immune-competent persons typically present as
mild, febrile illnesses that resemble infectious mononucleosis. Non-tender cervical or diffuse
lymphadenopathy may persist for weeks to months. Systemic findings may include fever, malaise,
headache, sore throat, rash, myalgias, hepatosplenomegaly, and atypical lymphocytosis. Rare severe
manifestations are pneumonitis, meningoencephalitis, hepatitis, myocarditis, polymyositis, and
retinochoroiditis. Symptoms may fluctuate, but most patients recover spontaneously within at most a
few months.

2. Congenital infection—Congenital transmission occurs as a result of infection, which may be

symptomatic or asymptomatic, in a non-immune woman during pregnancy. Fetal infection follows
maternal infection in 30–50% of cases, but this risk varies by trimester: 10–25% during the first, 30–
50% during the second, and 60% or higher during the third trimester. In the United States, an estimated
400 to 4000 congenital infections occur yearly. While the risk of fetal infection increases, the risk of
severe fetal disease decreases over the course of pregnancy. Early fetal infections commonly lead to
spontaneous abortion, stillbirths, or severe neonatal disease, including neurologic manifestations.
Neurologic findings can include seizures, psychomotor retardation, deafness, and hydrocephalus.
Retinochoroiditis and other sight-threatening eye lesions may develop. Systemic findings include fever
or hypothermia, jaundice, vomiting, diarrhea, hepatosplenomegaly, pneumonitis, myocarditis, and
rash. Infections later in pregnancy less commonly lead to major fetal problems. Most infants appear
normal at birth, but they may have subtle abnormalities and progress to symptoms and signs of
congenital toxoplasmosis later in life. Hepatosplenomegaly and lymphadenopathy may develop in the
first few months of life; CNS and eye disease often present later. The most common late presentation
of congenital toxoplasmosis is retinochoroiditis.

3. Retinochoroiditis—This manifestation of congenital toxoplasmosis presents weeks to years after

congenital infection, commonly in teenagers or young adults. Retinochoroiditis also is seen in persons
who acquire infection early in life, and these patients more often present with unilateral disease.
Uveitis is also seen. Disease presents with pain, photophobia, and visual changes, usually without
systemic symptoms. Signs and symptoms eventually improve, but visual defects may persist. Rarely,
progression may result in glaucoma and blindness.
4. Disease in the immunocompromised person—Reactivated toxoplasmosis occurs in patients with
AIDS, cancer, or those given immunosuppressive drugs. In patients with advanced AIDS, the most
common manifestation is encephalitis, with multiple necrotizing brain lesions. The encephalitis usually
presents sub-acutely, with fever, headache, altered mental status, focal neurologic findings, and other
evidence of brain lesions. Less common manifestations of toxoplasmosis in patients with AIDS are
chorioretinitis and pneumonitis. Chorioretinitis presents with ocular pain and alterations in vision.
Pneumonitis presents with fever, cough, and dyspnea. Toxoplasmosis can develop in seronegative
recipients of solid organ or bone marrow transplants due to reactivation or, more rarely, transmission
of infection. Reactivation also can occur in those with hematologic malignancies or treated with
immunosuppressive drugs. With primary or reactivated disease in those with immunodeficiency due to
malignancy or immunosuppressive drugs, toxoplasmosis is similar to that in individuals with AIDS,
but pneumonitis and myocarditis are more common.
JOURNAL OF CLINICAL MICROBIOLOGY, Oct. 1996, p. 2368–2371 Vol. 34, No. 10
0095-1137/96/$04.0010
Copyright q 1996, American Society for Microbiology

Urine Sample Used for Congenital Toxoplasmosis Diagnosis by PCR

ISABEL FUENTES,1* MERCEDES RODRIGUEZ,1 CARLOS J. DOMINGO,1 FERNANDO DEL
CASTILLO,2
TERESA JUNCOSA,3 AND JORGE ALVAR1
Received 1 February 1996/Returned for modification 5 March 1996/Accepted 8 July 1996

The diagnosis of toxoplasmosis in congenitally infected infants can be difficult; serology is

unreliable, and diagnosis must be based on the combination of symptomatology and direct
demonstration of the parasite. Four infants suspected of having Toxoplasma gondii infection were
studied by serological analysis, tissue culture, and PCR determination. T. gondii was isolated from the
urine of one patient. The parasite was detected by PCR in the blood and cerebrospinal fluid of three
infants and in the urine in all patients. Because nested PCR proved to be a sensitive, relatively rapid,
and specific method and because it can be applied to a variety of different clinical samples, PCR can
be a valuable technique for the identification of T. gondii infections in children. The present study
indicates that PCR examination of urine, a fluid never before used for diagnosis in this age group, may
be valuable in diagnosing cases of congenital toxoplasmosis.

Amebiasis
Essentials of diagnosis
1. Organisms or antigen present in stools or abscess aspirate.
2. Positive serologic tests with colitis or hepatic abscess, but these may represent prior
infections.
3. Mild to moderate colitis with recurrent diarrhea.
4. Severe colitis including bloody diarrhea, fever, and abdominal pain, with potential
progression to hemorrhage or perforation.
5. Hepatic abscess with fever, hepatomegaly, and abdominal pain.
``
General Considerations
The Entamoeba complex contains three morphologically identical species: Entamoeba dispar
and Entamoeba moshkovskii, which are avirulent, and Entamoeba histolytica, which may be an
avirulent intestinal commensal or lead to serious disease. Disease follows penetration of the intestinal
wall, resulting in diarrhea, and with severe involvement, dysentery or extraintestinal disease, most
commonly liver abscess. E histolytica infections are present worldwide but are most prevalent in
subtropical and tropical areas under conditions of crowding, poor sanitation, and poor nutrition. Of the
estimated 500 million persons worldwide infected with Entamoeba, most are infected with E dispar
and an estimated 10% with E histolytica. The prevalence of E moshkovskii is unknown. Mortality from
invasive E histolytica infections is estimated at 100,000 per year. Humans are the only established E
histolytica host. Transmission occurs through ingestion of cysts from fecally contaminated food or
water, facilitated by personto-person spread, flies and other arthropods as mechanical vectors, and use
of human excrement as fertilizer. Urban outbreaks have occurred because of common-source water
contamination.
Clinical Findings
A. Symptoms and Signs
1. Intestinal amebiasis—In most infected persons, the organism lives as a commensal, and the carrier
is without symptoms. With symptomatic disease, diarrhea may begin within a week of infection,
although an incubation period of 2–4 weeks is more common, with gradual onset of abdominal pain
and diarrhea. Fever is uncommon. Periods of remission and recurrence may last days to weeks or
longer. Abdominal examination may show distention, tenderness, hyperperistalsis, and hepatomegaly.
Microscopic hematochezia is common. More severe presentations include colitis and dysentery, with
more extensive diarrhea (10–20 stools per day) and bloody stools. With dysentery, physical findings
include high fevers, prostration, vomiting, abdominal pain and tenderness, hepatic enlargement, and
hypotension. Severe presentations are more common in young children, pregnant women, those who
are malnourished, and those receiving corticosteroids. Thus, in endemic regions, corticosteroids should
not be started for presumed inflammatory bowel disease without first ruling out amebiasis. Fulminant
amebic colitis can progress to necrotizing colitis, intestinal perforation, mucosal sloughing, and severe
hemorrhage, with mortality rates over 40%. More chronic complications of intestinal amebiasis include
chronic diarrhea with weight loss, which may last for months to years; bowel ulcerations; and amebic
appendicitis. Localized granulomatous lesions (amebomas) can present after either dysentery or
chronic intestinal infection. Clinical findings include pain, obstructive symptoms, and hemorrhage and
may suggest intestinal carcinoma.

2. Extraintestinal amebiasis—The most common extraintestinal manifestation is amebic liver

abscess. This can occur with colitis, but more frequently presents without history of prior intestinal
symptoms. Patients present with the acute or gradual onset of abdominal pain, fever, an enlarged and
tender liver, anorexia, and weight loss. Diarrhea is present in a small number of patients. Physical
examination may show intercostal tenderness. Abscesses are most commonly single and in the right
lobe of the liver, and they are much more common in men. Without prompt treatment, amebic
abscesses may rupture into the pleural, peritoneal, or pericardial space, which is often fatal. Amebic
infections may rarely occur throughout the body, including the lungs, brain, and genitourinary system.

Giardiasis
Essentials of diagnosis
1. Acute diarrhea; may be profuse and watery.
2. Chronic diarrhea with greasy, malodorous stools.
3. Abdominal cramps, distention, flatulence, and malaise.
4. Cysts or trophozoites in stools.

General Considerations
Giardiasis is a protozoal infection of the upper small intestine caused by the flagellate Giardia lamblia
(also called Giardia intestinalis and Giardia duodenalis). The parasite occurs worldwide, most
abundantly in areas with poor sanitation. In developing countries, young children are very commonly
infected. In the United States and Europe, the infection is the most common intestinal protozoal
pathogen; the US estimate is of 100,000 to 2.5 million new infections leading to 5000 hospital
admissions yearly. Groups at special risk include travelers to Giardia-endemic areas, those who
swallow contaminated water during recreation or wilderness travel, men who have sex with men, and
persons with impaired immunity. Outbreaks are common in households, children’s day care centers,
and residential facilities, and may occur as a result of contamination of water supplies. The organism
occurs in feces as a flagellated trophozoite and as a cyst. Only the cyst form is infectious by the oral
route; trophozoites are destroyed by gastric acidity. Humans are a reservoir for the pathogen; dogs,
cats, beavers, and other mammals have been implicated but not confirmed as reservoirs. Under suitable
moist, cool conditions, cysts can survive in the environment for weeks to months. Cysts are transmitted
as a result of fecal contamination of water or food, by person-to-person contact, or by anal-oral sexual
contact. The infectious dose is low, requiring as few as ten cysts. After the cysts are ingested,
trophozoites emerge in the duodenum and jejunum. Epithelial damage and mucosal invasion are
uncommon. Hypogammaglobulinemia, low secretory IgA levels in the gut, achlorhydria, and
malnutrition favor the development of infection.

Clinical Findings
A. Symptoms and Signs
It is estimated that about 50% of infected persons have no discernable infection, about 10% become
asymptomatic cyst passers, and 25–50% develop an acute diarrheal syndrome. Acute diarrhea may
clear spontaneously but is commonly followed by chronic diarrhea. The incubation period is usually
1–3 weeks but may be longer. The illness may begin gradually or suddenly. Cysts may not be detected
in the stool at the onset of the illness. The acute phase may last days or weeks, and is usually self-
limited, although cyst excretion may be prolonged. The initial illness may include profuse watery
diarrhea, and hospitalization may be required due to dehydration, particularly in young children.
Typical symptoms of chronic disease are abdominal cramps, bloating, flatulence, nausea, malaise, and
anorexia. Fever and vomiting are uncommon. Diarrhea is usually not severe in the chronic stage of
infection; stools are greasy or frothy and foul smelling, without blood, pus, or mucus. The diarrhea
may be daily or recurrent; intervening periods may include constipation. Symptoms can persist for
weeks to months. Weight loss is frequent. Chronic disease can include malabsorption, including fat-
and protein-losing enteropathy and vitamin deficiencies.

Trichomoniasis
Essentials of diagnosis
1. Copious vaginal discharge in women.
2. Nongonococcal urethritis in men.
3. Motile trichomonads on wet mounts.

General Considerations
Trichomoniasis is caused by the protozoan Trichomonas vaginalis and is among the most common
sexually transmitted diseases, causing vaginitis in women and nongonococcal urethritis in men. It can
also occasionally be acquired by other means, since it can survive in moist environments for several
hours.

Clinical Findings
A. Symptoms and Signs
T vaginalis is often harbored asymptomatically. For women with symptomatic disease, after an
incubation period of 5 days to 4 weeks, a vaginal discharge develops, often with vulvovaginal
discomfort, pruritus, dysuria, dyspareunia, or abdominal pain. Examination shows a copious discharge,
which is usually not foul smelling but is often frothy and yellow or green in color. Inflammation of the
vaginal walls and cervix with punctate hemorrhages are common. Most men infected with T vaginalis
are asymptomatic, but it can be isolated from about 10% of men with nongonococcal urethritis. In men
with trichomonal urethritis, the urethral discharge is generally more scanty than with other causes of
urethritis.

CHROMOBLASTOMYCOSIS (Chromomycosis)
Chromoblastomycosis is a chronic, principally tropical cutaneous infection usually affecting young
men who are agricultural workers and caused by several species of closely related black molds;
Cladophialophora carrionii and Fonsecaea pedrosoi are the most common etiologic agents. Lesions
usually follow puncture wounds and are slowly progressive, occurring most frequently on a lower
extremity. The lesion begins as a papule or ulcer. Over months to years, papules enlarge to become
vegetating, papillomatous, verrucous elevated nodules. Satellite lesions may appear along the
lymphatics. There may be secondary bacterial infection. Elephantiasis may result. The fungus is seen
as brown, thick-walled, spherical, sometimes septate cells in potassium hydroxide preparations of pus
or skin scrapings, which are quite sensitive for diagnosis. The type of reproduction found in culture
determines the species. Itraconazole, 200–400 mg/d orally for 6–18 months, achieves a response rate
of 65%. Terbinafine at 500–1000 mg/d orally may have similar efficacy to itraconazole and may be
useful in combination, especially in difficult to treat cases. Cryosurgery alone for smaller lesions or
combined with itraconazole for larger lesions is beneficial.

MYCETOMA (Maduromycosis & Actinomycetoma)

Mycetoma is a chronic local, slowly progressive destructive infection, usually involving the foot, that
begins in subcutaneous tissues, frequently after localized trauma, and then spreads to contiguous
structures. Maduromycosis (also known as eumycetoma) is the term used to describe mycetoma caused
by the true fungi and by phylogenetically diverse organisms. Actinomycotic mycetoma is caused by
Nocardia and Actinomadura species. The disease begins as a papule, nodule, or abscess that over
months to years progresses slowly to form multiple abscesses and sinus tracts ramifying deep into the
tissue. Secondary bacterial infection may result in large open ulcers. Radiographs may show
destructive changes in the underlying bone. Tissue Gram stain reveals fine branching hyphae with
actinomycotic mycetoma. Larger hyphae are seen with fungal mycetoma; the causative species can
often be identified by the color of the characteristic grains within the infected tissues. The prognosis is
good for patients with actinomycetoma, since they usually respond well to sulfonamides and sulfones,
especially if treated early. TMP-SMZ, 160/800 mg orally twice a day, or dapsone, 100 mg twice daily
after meals, has been reported to be effective. Streptomycin, 14 mg/kg/d intramuscularly, may be
useful during the first month of therapy. All oral medications must be taken for months and continued
for several months after clinical cure to prevent relapse. Debridement assists healing. The prognosis for
maduromycosis is poor, though surgical debridement along with prolonged itraconazole therapy
may result in a response rate of 70%. The various etiologic agents may respond differently to
antifungal agents, so culture results are invaluable. Amputation is necessary in far advanced cases.

Sumber:
a. Kasper DL, et al. (Editors). 2005. Harrison’s Principles of Internal Medicine. 16th Ed.
b. Papadakis MA and McPhee SJ. 2013. Current Medical Diagnosis and Treatment.
c. Kantele A and Jokiranta TS. 2011. Review of Cases With the Emerging Fifth Human Malaria
Parasite, Plasmodium knowlesi. CID. 52(11).

Actinomycosis
Actinomycosis was once a common & ultimately fatal disease. Now the number has declined since the
introduction of antimicrobial agents. The outlook of patients suffering from this infection has improved
remarkably. Few physicians see many cases. As patients no longer commonly present advanced
disease, actinomycosis has become a more diagnostic challenge. Actinomycosis is a subacute-
tochronic bacterial infection characterized by contiguous spread, suppurative and granulomatous
inflammation, and formation of multiple abscesses and sinus tracts that may discharge ‘sulfur
granules’. As a disease process, the causative organism can primarily or secondarily invade gum, jaw,
neck, pleura, lungs, liver, kidney, appendix, caecum, skin, heart, meninges etc. Even bones like
mandible, ribs & vertebra (causing osteomyelitis) are not immune to its invasion. The most common
clinical forms of actinomycosis are cervicofacial (ie, lumpy jaw), thoracic, and abdominal. In women,
pelvic actinomycosis is documented. Epidural abscesses, meningitis, Endocaditis, Pericarditis,
Pneumonia (Community Acquired or Nosocomia), Lung absecess, Bronchiectasis, Empyema Thoracis
etc when caused by these organisms remain undiagnosed or if not properly treated would endanger the
life of the patient. There are significant morbidities as well.

Aetiology
The causative organisms are non-motile, non-spore forming, non-acid fast, Gram positive
pleomorphic, anaerobic-tomicroaerophilic filamentous bacterial rods. The most common ones are
Actinomyces israeli, Actinomyces gerencseriae, Actinomyces naeslundii, Actinomyces odontolyticus,
Actinomyces viscosus, Actinomyces turicensis, Actinomyces meyeri, Propionibacterium propionicus.
In addition to these microorganisms, almost all actinomycotic lesions contain so-called companion
bacteria. The most important of these bacteria is Actinobacillus actinomycetemcomitans, followed by
Peptostreptococcus, Prevotella, Fusobacterium, Bacteroides, Staphylococcus, and Streptococcus
species, and Enterobacteriaceae, depending on the location of actinomycotic lesions. These companion
bacteria appear to magnify the low pathogenic potential of actinomycetes. Actinomycosis can affect
people of all ages, but the majority of cases are reported in young to middle-aged adults (aged 20-50
yrs). No racial predilection exists. For unknown reasons, men are affected more commonly than
women, with the exception of pelvic actinomycosis. The reported male-to-female ratio is 3:1.
Actinomycosis occurs worldwide, with likely higher prevalence rates in areas with low socioeconomic
status and poor dental hygiene. (Moniruddin ABM1, Begum H2, Nahar K3. 2010. Medicine Today. p
43)