Tropical Infection Disease - Lecture2

GSH - Tropmed - 2010
TROPICAL INFECTION DISEASES

Gatot Sugiharto, MD, Internist Internal Medicine Department Faculty of Medicine, Wijaya Kusuma University Surabaya
LEPTOSPIROSIS
Introduction
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Leptospirosis is an acute anthropo-zoonotic infection
Occurs in tropical, subtropical and temperate zones. Synonym : Weil Disease, Hemorrhagic Jaundice, Mud Fever, Swineherd Disease, Canicola Fever, seven-day fever (commonly in Japan), Cane cutters disease (in Australia), Rice field Leptospirosis (in Indonesia) , Fort Bragg fever in U.S.Andaman haemorrhagic fever (AHF)
Leptospirosis
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Caused by spirochete bacteria leptospira, a thin spiral organism It is characterized by very active motility, by rotating (spinning) and bending. Usually one or both ends of this singlecell organism are bent or hooked >250 serovars L. Interrogans L. canicola L. hardjo L. pomona L. icterohaemorrhagiae
High risk occupations

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Rice/taro farming Mining Sewage/canal work Cane harvesting Fish farming

Route of Transmission
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Main resevoir : rodents, livestock (cattle, horses, sheep, goats, swine), canines, and wild mammals Replicates in renal tubules, excreted in urine Human infection occurs with direct contact with infected urine, or indirect exposure to organisms in wet soil & water, rarely by droplet inhalation Often results from occupational exposure to ratinfected water
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Mechanism of Disease
Systemic vasculitis occurs, facilitating migration of spirochetes into organs

Hepatocellular Acute
damage with jaundice, inc INR
tubular necrosis of kidney
Increased
capillary fragility hemorrhage can occur in any internal organ (pulmonary hemorrhage)
Scanning electron microscopy of a renal tubule from an experimentally infected rat

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Clinical Presentation(1)
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Incubation period: 2-20 days (median 11 days) Two types of leptospirosis:
Anicteric
leptospirosis or self-limited illness (85 -
90% ) Icteric leptospirosis (5 - 10% )
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Symptoms:
Clinical Presentation : early phase (4-7 days)
HA, myalgia, chills, back pain, anorexia, sore throat nausea/vomiting Hemoptysis, cough, SOB
Signs:
Acute febrile illness (40oC) Conjunctival suffusion Nontender transient pretibial raised erythematous patches Hepatomegaly Meningitis
Labs: thrombocytopenia, proteinuria, elevated WBC

Clinical Presentation: Late Phase

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Second (Immune) phase: day 7+ Patient develops antibodies to the organism Meningitis or hepatorenal manifestations more prominent Fevers may subside, becomes more jaundiced, can bleed into skin, mucous membranes, lungs Oligouric renal failure, shock, myocarditis, arrythmias can follow
Weils Disease
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Severe form of leptospirosis Described by Weil in 1886 as a clinical syndrome in 4 men with severe jaundice, fever, hemorrhage, and renal involvement Inada et al identified the causal agent in Japan in 1916 Most severe cases, with hepatorenal involvement and jaundice, can have a mortality rate of 20-40%
Diagnosis
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Direct visualization of leptospires in blood (early phase) or urine (late phase) by darkfield microscopic examination

Low sensitivity (40.2%) and specificity (61.5%) Need special media (Fletcher's, Ellinghausen's, polysorbate ) Takes 2-3 weeks to be positive Microscopic agglutination test (MAT), ELISA Titer >1:100 helps, but fourfold rise in titer is diagnostic (need convalescent sample)
IgM antibodies appear in late phase (5-7 days)

Diagnostic Tests for Leptospirosis
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Differential diagnosis
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Influenza Meningitis (encephalitis) Viral hepatitis Rickettsiosis Typhoid fever Septicemia Toxoplasmosis Legionnaires disease Malaria
Treatment
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IV penicillin for severe disease Oral amoxycillin, erythromycin, doxycycline for mild illness (10-14 d) Jarisch-Herxheimer reactions have been reported in patients treated with penicillin Prognose Humans with leptospirosis usually excrete the organism in the urine for 4-6 weeks and occasionally for as long as 18 weeks.
Prevention
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Rodent control measures Immunization of animals with killed vaccines shortlived, requires boosters Protective clothing, footwear Burning canefield prior to harvest (young shoots can cut hands) Drink boiled water Doxycycline prophylaxis for high-risk workers
COMPLICATIONS
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Azotemia Oliguria Hemorrhage Purpura Hemolysis Gastrointestinal bleeding Hypoprothrombinemia & thrombocytopenia
Fort Bragg Fever

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August 1942, an unusual acute febrile illness (99.8 to 105.6F) occurred in a group of soldiers at Fort Bragg, N.C. Soldiers quartered near a small stream and its tributaries 40 patients with sudden onset malaise, mild aches, lumbar pain, severe headaches Bilaterally symmetrical rash limited in to the pretibial areas on the fourth day Similar outbreaks 1946 and 1947 among soldiers quartered in the same area of the post
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MALARIA
Introduction
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The protozoan genus Plasmodium is responsible for malaria Four important species: Plasmodium falciparum, P. vivax, P. malariae and P. ovale Rapidly fatal and is responsible for most malaria related deaths : P. Falciparum Mosquito-transmitted malaria is the greatest public health problem in large parts of the world with more than 500 million clinical cases and over 3 million deaths every year
Epidemiology
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Occurs in most of the tropics of the world
Prevalence of falciparum and vivax malarias being

about the same in Asia, Oceania and South America
Malaria can be a travelers disease and imported

into any country.
A rural disease due to the presence of the female
Anopheles mosquito vector.

Tranmission
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Transmision : by an infected female
Anopheles biting
Others : blood transfusion or congenitally feto-maternal Malaria-carrying Anopheles bite only near dusk and dawn.
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Clinical manifestation on life cycle.

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Plasmodia replicate inside the RBC hemoliysis release of toxic metabolic by products into the bloodstream. These symptoms include chills, headache, myalgias and malaise, occurring in cycles. Also may cause splenomegaly, jaundice and anemia P falciparum may induce kidney failure, coma and death.
Chronic & relapse

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All infected liver cells parasitized with P. falciparum and P. malariae rupture and release merozoites at about the same time. In contrast, P. vivax and P. ovale have two exoerythrocytic forms. The primary type develops, causes liver cell rupture, and releases merozoites. The other form, which develops concurrently, is known as the hypnozoite. Sporozoites that enter liver cells differentiate into nonsexual hypnozoites that remain dormant for weeks, or even years. The hypnozoites activate and undergo exoerythrocytic schizogony, forming a wave of merozoites that cause a relapse. GSH - Tropmed - 2010
Clinical symptoms(1)
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Cough, fatigue, malaise, arthralgia, myalgia, and paroxysm of shaking chills and sweats The classic paroxysm : begins with shivering and chills, (1-2 hours) followed by high fever Paroxyms of varying 48 hours belong to vivax, ovale and falciparum malaria, whereas 72 hours belongs to malariae infections. The 48 hour fever is called tertian (occurs every 3rd day) day 1 : fever, day 2 : no fever, day 3 : fever & so on. The 72 hour fever is called quartan (returns on every 4th day) GSH - Tropmed - 2010
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30% of non-immune adults infected with P falciparum suffer acute renal failure, some with seizures. Blackwater fever : hemoglobinuria with the passage of dark-colored urine Non-cardiogenic pulmonary edema :common in pregnant women and results in death in 80% of patients Profound hypoglycemia : young children and pregnant women. The most prominent symptoms all relate to loss of RBCs: a) tachycardia, b) anemia, c) fever, d) hypotension and e) splenomegaly.
Severe malaria
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1. Cerebral malaria 2. Acute renal failure 3. ARDS 4. Severe anaemia (Hb < 5g%) 5. DIC 6. Haemoglobinuria 7. Hypotension, Shock 8. Hyperparasitemia 9. Repeated seizures 10. Hyperpyrexia 11. Haemolysis (Sr bil. >3 mg%)
Cerebral malaria
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The principal signs : seizures and unconsciousness, preceded by a severe headache. Neurologic examination : contracted or unequal pupils, a Babinski sign, and absent or exaggerated deep tendon reflexes Cerebrospinal fluid examination : increased pressure, increased protein, and minimal or no pleocytosis. High fever, 41 to 42C, with hot, dry skin may occur.
ARDS
35
Often fatal, develop rapidly, associated with excessive intravenous fluid therapy. Fast, labored respiration, SOB, a nonproductive cough, rales and rhonchi Chest X-rays : increased bronchovascular markings.
Confirmed Diagnosis of Malaria

36
All clinically suspected malaria cases require laboratory examination and confirmation. Only in case where laboratory confirmation is not possible start treatment immediately. Parasitological confirmation is done by thin-thick blood smear microscopy examination or by dipstick (Rapid Diagnostic Test [RDT]) or by serologic test (ICT)
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38
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Figure 1. Morphology of Plasmodium knowlesi in a Giemsa-stained thin blood smear. Infected erythrocytes were not enlarged, lacked Schuffner stippling, and contained much pigment. Shown are examples of trophozoites (AF), a schizont (G), and a gametocyte (H). Scale bars = 5 m.
Malaria Therapy
Plasmo dium Un known Falci parum Condition Non pregnant Pregnant Sensitive Chloroquin Resisten Chloroquin < 25% 1st reg Chloroquin Primaquin Chloroquin Chloroquin Primaquin Chloroquin SP Primaquin Formula 4-4-2 3 4-4-2 4-4-2 3 4-4-2 3 3 2nd reg Kina Primaquin Kina SP Primaquin Formula 3x2 (7) 2-3 3x2 (7) 3 2-3 Kina Primaquin 3x2 (7days) 2-3 3rd reg/ relaps Formula
Resisten Chloroquin >25%

Resisten SP >25% Resinten both SP+C
Kina Primaquin
Chloroquin Tetra/doxy Primaquin Kina Tetra/doxy Primaquin
3x2 (7) 3
4-4-2 4x2/2x1 (7) 3 3x2 (7) 4x2/2x1 (7) 3
SP Tetra/doxy Primaquin
Chloroquin Kina Primaquin
3 4x2/2x1 (7) 3
4-4-2 3x2 (7) 3
CI for pregnancy, infant : Primaquin, SP

40
Plasmo dium
Vivax/ ovale
Condi tion
1st reg
Chloroquin Primaquin
Formula
4-4-2 1 (14) 4-4-2 4x2/2x1 (7) 1 (14) 3x2 (7) 4x2/2x1 (7) 1 (14)
2nd reg
Kina Primaquin
Formula
3x2 (7) 1
3rd reg/ relaps

Chloroquin Primaquin
Formula
4 (8-12 week) 3 (8-12 week)
Resisten Chloroqui n < 25% Resisten Chloroqui n >25%
Chloroquin Tetra/doxy Primaquin Kina Tetra/doxy Primaquin
Aim
Prophylaxis
Regimen
Chloroquin
Dose
2 tabs/week
Condition
Temporary visitation
Permanent visitation
Duration
1 week before 4 week after visitation
Max for 3 months Max for 3 months
Doxycycline
1.5 mg/kg/day
Only for Chloroquin resistan Falciparum GSH - Tropmed - 2010
41
Monitoring Malaria Treatment
Early Tx failure
Late Tx failure
H1-3 show sign of severe malaria H2 parasite count > H0 H3 parasite count > 25% H0 H3 sexual parasite still (+) or temp >37.5
Late clinical failure
In 4th-28th shows sign of severe malaria Sexual parasite still (+) or temp >37.5 Sexual parasite still (+) in 7th, 14th, 21st, 28th day or temp > 37.5
Late parasitologic failure
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Artemicin based combined therapy (ACTs) for uncomplicated falciparum malaria

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The following ACTs are recommended:

artemether-lumefantrine artesunate
- amodiaquine artesunate + mefloquine artesunate + sulfadoxine-pyrimethamine dihydroartemisinin piperaquine
The artemisinin derivatives (oral formulations) and partner medicines of ACTs should not be used as monotherapy in the treatment of uncomplicated malaria
*Update in 2009 WHO Revised Guidelines
Uncomplicated malaria treatment

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P. falciparum malaria The treatment of uncomplicated P. falciparum malaria is undertaken after diagnosis of malaria by light microscopy or Dipstick. Patients with positive think-thick blood smears or dipstick for P. falciparum malaria is treated by blisters of Coartem (artemether 20mg/lumefantrine 120mg). See Table 1 for details of prescription.
Coartem Dosage Schedule

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Source: WHO, 2007
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TOXOPLASMOSIS
Definition
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Toxoplasmosis is a zoonotic infection caused by a microscopic parasite Toxoplasma gondi. These microscopic parasites live inside the cells of humans and animals Domestic cat and other Felidae are the definitive host Vertebrates are the intermediate host
Amphibians, fish, reptiles, All warm-blooded animals including man
Toxoplasma - organelles
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Epidemiology
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Toxoplasmosis is one of the most common infections in the world. About 60 million people in the United States get it. 400 to 4000 babies are born with congenital toxoplasmosis each year. 90% of the babies born with it have no symptoms in infancy. 1 in 10 babies show symptoms when born 85% of babies show symptoms months to years later.
Transmision
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By touching or coming into contact with infected cat feces.
By eating contaminated raw or undercooked meat.

By eating contaminated unwashed fruits or vegetables. By passing it to your unborn baby. By organ transplant or blood transfusion
Human/Congenital Transfer
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Toxoplasma gondii Life cycle

Oocyst Bradyzoite
Tachyzoite
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T. gondii life cycle (cont.)
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Toxoplasmosis Cycle
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Toxoplasmosis in Humans
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Majority of cases are asymptomatic Mild fever, sore muscles swollen glands and lymph nodes, similar to mononucleosis Immunocompromized individuals are at greater risk. HIV patients, Organ transplant patients, people on chemotherapy Pregnant womens fetus are at risk if the mother acquires the infection during gestation. CDC estimates 400-4000 cases of congenital toxoplasmosis per year. Blindness, Hydrocephalus, seizures and mental retardation are common 750 human deaths per year make it the 3rd most common lethal food poisoning.
SYMPTOMS OF TOXMOPLASMOSIS IN CHILDREN

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Toxoplasmosis can cause premature birth or stillbirth. In most cases newborns do no show any noticeable symptoms. Babies born with severe toxoplasmosis usually have: eye infections, enlarged liver and spleen, jaundice, and pneumonia, some may die after birth. Babies who survive having severe toxoplasmosis can develop: mental retardation, impaired eyesight, cerebral palsy, seizures, and hearing loss.
Toxoplasmosis Diseases
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CONGENTIAL TOXOPLASMOSIS
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When a pregnant woman gets the infection during pregnancy and passes it on to her fetus. Women who get toxoplasmosis before conception hardly ever pass the infection during pregnancy. Babies that get infected during the first trimester show to have the most severe symptoms.
DURATION
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Toxoplasmosis can multiply and spread within a week as soon as the person gets infected, but it can take weeks or months before the person gets the symptoms. Toxoplasmosis is not curable, it stays in the persons body for life, but will remain inactive causing no harm. (life long immune protection) If the persons immune system is not working correctly due to HIV or cancer therapy, toxoplasmosis can be reactivated and cause serious harm. (nervous system)
Diagnosing Toxoplasmosis
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Detecting oocysts in the stool
Serological TestingELISA tests

IGg and IGm Titers of IgG can last for years Titers of IgM usually persist for only 12 weeks
Toxoplasmosis - Diagnosis
Antibody testing may be Followed by prenatal PCR or by CT or MRI scans
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Antibody testing
DIAGNOSIS DURING PREGNANCY

63
Ultra sounds can be done to diagnose congenital toxoplasmosis (but are not always 100% accurate) Get blood samples to measure the level of antibodies, which are the bodies defenses in the immune system. They have been new tests that can detect the DNA of the genes that have toxoplasmosis parasites. (these help detect congenital toxoplasmosis in the fetus)
TREATMENT DURING PREGNANCY

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Early diagnosis and prevention can greatly decrease the chances of the baby getting the infection badly, but will not reduce the chances of transmitting the infection from mother to child. If the pregnant woman is believed to have the infection active and she is in her first trimester of pregnancy : spiramycin. (Studies show that using spiramycin can reduce the chance of the fetus
getting infected by 60%)
If the fetus is infected, and the mother is 18 weeks gestation or more : pyrimethamine and sulfadiazine. (to reduce the newborns symptoms)
Toxoplasmosis - Treatment
Sulfadiazine and Pyrimethamine (Fansidar) usually given AIDS patients on antiretrovirals may modify depending on CD4 counts Patients allergic to sulfa drugs may take Clindamycin, Atovaquone, Clarithromycin, Azithromycin or Dapsone Leucovorin (Folinic acid) may be given with Pyrimethamine if blood counts are lowered
65 GSH - Tropmed - 2010
TREATMENT FOR INFECTED NEWBORNS

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Babies that are born with toxoplasmosis are also giving pyrimethamine and sulfadiazine. (first year of life or sometimes longer) 72% of infected babies had normal intelligence and motor function in their adolescence, but showed that eye infections reappeared Some babies still developed disabilities even after using the two medications, because of damages done before birth. In most cases babies are born without symptoms and therefore do not receive early treatment and developing severe disorders
PREVENTION OF TOXOPLASMOSIS
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Do not eat raw or undercooked meat
Wash hands after handling raw meat

Clean utensils, cutting boards, or other things that have come in contact with raw meats. Wash and peel fruits and vegetables Do not empty or clean cats litter boxes (if you do use gloves and wash hands after cleaning it) Try to keep your cats indoors to stop them from eating any animal that has been infected with parasites. Use gloves when gardening (soil may have parasites from cats.

Tropical Infection Disease - Lecture2

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GSH - Tropmed - 2010

TROPICAL INFECTION DISEASES

GSH - Tropmed - 2010

Leptospirosis is an acute anthropo-zoonotic infection

GSH - Tropmed - 2010

GSH - Tropmed - 2010

High risk occupations

Rice/taro farming Mining Sewage/canal work Cane harvesting Fish farming

GSH - Tropmed - 2010

GSH - Tropmed - 2010

GSH - Tropmed - 2010

Systemic vasculitis occurs, facilitating migration of spirochetes into organs

damage with jaundice, inc INR

tubular necrosis of kidney

Scanning electron microscopy of a renal tubule from an experimentally infected rat

GSH - Tropmed - 2010

Incubation period: 2-20 days (median 11 days) Two types of leptospirosis:

leptospirosis or self-limited illness (85 -

90% ) Icteric leptospirosis (5 - 10% )

GSH - Tropmed - 2010

Clinical Presentation : early phase (4-7 days)

Labs: thrombocytopenia, proteinuria, elevated WBC

Clinical Presentation: Late Phase

GSH - Tropmed - 2010

GSH - Tropmed - 2010

IgM antibodies appear in late phase (5-7 days)

Diagnostic Tests for Leptospirosis

GSH - Tropmed - 2010

GSH - Tropmed - 2010

GSH - Tropmed - 2010

Fort Bragg Fever

GSH - Tropmed - 2010

GSH - Tropmed - 2010

Occurs in most of the tropics of the world

Prevalence of falciparum and vivax malarias being

Malaria can be a travelers disease and imported

A rural disease due to the presence of the female

Anopheles mosquito vector.

Transmision : by an infected female

GSH - Tropmed - 2010

GSH - Tropmed - 2010

GSH - Tropmed - 2010

Clinical manifestation on life cycle.

Chronic & relapse

GSH - Tropmed - 2010

GSH - Tropmed - 2010

Confirmed Diagnosis of Malaria

GSH - Tropmed - 2010

GSH - Tropmed - 2010

GSH - Tropmed - 2010

Resisten Chloroquin >25%

GSH - Tropmed - 2010

CI for pregnancy, infant : Primaquin, SP

3rd reg/ relaps

Resisten Chloroqui n < 25% Resisten Chloroqui n >25%

Chloroquin Tetra/doxy Primaquin Kina Tetra/doxy Primaquin

Only for Chloroquin resistan Falciparum GSH - Tropmed - 2010

Monitoring Malaria Treatment

Late clinical failure

Late parasitologic failure

GSH - Tropmed - 2010

Artemicin based combined therapy (ACTs) for uncomplicated falciparum malaria