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Tropical Infection Diseases

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1 Tropical Infection Diseases
Gatot Sugiharto, MD, Internist Internal Medicine Department Faculty of Medicine, Wijaya Kusuma University Surabaya GSH - Tropmed

2 DENGUE FEVER/DENGUE HEMORHAGIC FEVER
Gatot Sugiharto, MD, Internist Internal Medicine Department Faculty of Medicine, Wijaya Kusuma University Surabaya GSH - Tropmed

3 Introduction(1) Dengue fever is a clinical illness with symptoms ranging from a nonspecific viral syndrome such as fever, severe headache, sore throat, rash, and muscle pain, and joint pain, to severe and fatal hemorrhagic Primarily a disease of the tropics, and the viruses that cause it are maintained in a cycle that involves humans and Aedes aegypti, a domestic, day-biting mosquito that prefers to feed on humans

4 Introduction(2) Dengue is one of the most important mosquito-born viral diseases affecting humans. Viral life cycle involves humans and the mosquito vector Aedes aegypti, some others by Aedes albopictus The disease is caused by 4 serotypes of the Dengue virus, a member of the genus RNA- Flavivirus: DEN-1, DEN-2, DEN-3, DEN-4. Infection with the DEN virus can result in Dengue Fever (DF), Dengue Hemorrhagic Fever (DHF) and Dengue Shock Syndrome (DSS). It has one of the largest geographic spread of any known virus (exception is HIV). A. aegypti: domestic, day-biting mosquitoes that primarily feed on humans and the DEN virus is transmitted during the feeding process. They also transmit Yellow Fever Virus (In the 1950s the World Pan Health Organization tried to eradicate A. aegypti in order to combat urban Yellow Fever (using DDT). They pulled out in 1970s and by 1997 the geographic spread of the mosquito was larger than before the eradication began). Infection with one serotype does not provide cross-protective immunity, in fact, it is thought that exposure to one serotype can make you more susceptible to infection by the other three (multiple serotype infection leads to DHF- time constraints associated with this). There is a 5% mortality rate associated with DHF in third world countries.

5 History The first suspected epidemics of dengue fever being reported during 1779 to 1780 in Asia, Africa, and North America. The dengue virus was first isolated in Japan in 1943, but this work was not immediately published. At the same time, Dr. Albert Sabin, working with the U. S. Army Commission on dengue and sandfly Fever, identified the dengue virus.

6 Global Spread of Dengue
It has been estimated that in recent years as many as 10 million cases of dengue fever and 500,000 cases of DHF/DSS occur annually. Case fatality rates in some countries reach 5% million infections/year Countries with active dengue + Aedes aegypti

7 FOUR VIRUSES Life time immunity follows infection to one type.
Second, third and possibly four infections are possible. CHILDREN – first infections are mild, largely inapparent. ADULTS - first infections may produce DF, some viruses more overt than others. The four dengue viruses, members of the flavivirus genus, evolved from a common ancestor in subhuman primates and separately were introduced into the urban transmission cycle.

8 Characteristics of the Aedes Mosquito
One distinct physical feature – black and white stripes on its body and legs. Bites during the day. Lays its eggs in clean, stagnant water. Close-up of an Aedes mosquito Now I’ll tell you about the Aedes mosquito which spreads dengue. 1) You can identify an Aedes mosquitoe from other mosquitoes by the black & white stripes on its body and legs. Because of this, it is also known as the ‘tiger mosquito. 2) It usually bites during the day. 3) The Aedes mosquito lays its eggs in clean, stagnant water. A pool of water as small as a twenty cent coin is all that is needed for it to breed. 

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10 1.The virus is inoculated into humans with the mosquito saliva.
2.The virus localizes and replicates in various target organs, for example, local lymph nodes and the liver. 3.The virus is then released from these tissues and spreads through the blood to infect white blood cells and other lymphatic tissues. 4.The virus is then released from these tissues and circulates in the blood. 5.The mosquito ingests blood containing the virus 6.The virus replicates in the mosquito midgut, the ovaries, nerve tissue and fat body. It then escapes into the body cavity, and later infects the salivary glands. 7.The virus replicates in the salivary glands and when the mosquito bites another human, the cycle continues.

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12 Pathogenesis

13 Pathogenesis

14 Symptoms A sudden onset of fever 3 – 5 days after bitten by a dengue- infected mosquito, usually continues for 2 to 7 days and can be as high as 104 to 106 ° Severe headache, muscle pain, joint pain, conjunctivitis, severe orbital pain, backache, anorexia, and nausea and vomiting Other symptoms : rash, minute reddish/purplish spots, nose bleeds, or bleeding gums. Hemorrhagic manifestations usually occur about the time that the body temperature falls back to or below normal During the hemorrhagic, signs of circulatory failure may appear. Evidence of a capillary leak syndrome : reduced blood volume (hypovolemia), shock, and death can follow. Prolonged fatigue and depression continue through the recovery stage.

15 Physical & lab finding

16 Dengue Disease Course Summary in Untreated Individuals
24 April 2017 Dengue Disease Course Summary in Untreated Individuals Day 1 Day 2 Day 3 Day 4 Day 5 Day 6 Day 7 Day 8 Day 9 Day 10 Day 11 Day 12 Day 13 Day 14 EXPOSURE Incubation 3-5 Days High fever, headache, etc. lasting 2 to 7 days Mortality rate for untreated DHF can be as high as 20% Dengue is caused by one of four closely related, but antigenically distinct, viral serotypes (DEN-1, DEN-2, DEN-3, and DEN-4) of the genus Flavivirus, family Flaviviridae. The severe hemorrhagic forms are called dengue hemorrhagic fever (DHF) and dengue shock syndrome (DSS). Severe cases of the disease appear to be associated with DEN-2 and DEN-3. Infection by one of these serotypes does not provide cross-protective immunity; persons living in a dengue-endemic area can contract all four dengue infections during their lifetimes. Epidemics of mass proportions occur, but fatalities are rare. Each year, tens of millions of cases of dengue fever occur and, depending on the year, up to hundreds of thousands of cases of DHF. The fatality rate of untreated DHF in most countries can be as high as 20 percent; however, with proper care, less than 1 to 2 percent of patients with dengue or DHF will die.  Most fatal cases are among children and young adults. A sudden onset of fever appears within 3 to 5 days of being bitten by a dengue-infected mosquito. Other symptoms include severe headache, muscle pain, joint pain, conjunctivitis, severe orbital pain, backache, anorexia, and gastrointestinal disturbances (nausea and vomiting in more severe cases). Other symptoms may include a rash, minute reddish/purplish spots, nose bleeds, or bleeding gums. The illness commonly begins with a sudden rise in temperature accompanied by facial flush.  The fever usually continues for 2 to 7 days and can be as high as 104 to 106 °F. Hemorrhagic manifestations usually occur about the time that the body temperature falls back to or below normal. During the hemorrhagic manifestation, signs of circulatory failure may appear. Platelet counts of less than 100,000/cubic millimeter (thrombocytopenia) and evidence of a capillary leak syndrome appears in clinical laboratory tests. Reduced blood volume (hypovolemia), shock, and death can follow. Prolonged fatigue and depression continue through the recovery stage. The references for the text are the Biological and Chemical Warfare Online Repository and Technical Holding System (BACWORTH), Version Battelle Memorial Institute, 1997 and the CDC website ( 18 June 2001

17 Diagnosis Clinical picture
24 April 2017 Diagnosis Clinical picture Detection of anti-dengue immunoglobulin (Ig) M or IgG antibody in a patient's blood serum Isolated from human blood after mosquito inoculation, or from mosquito cell cultures, by immunofluorescence using serotype-specific monoclonal antibodies (MAbs). Detection of dengue virus by culture is the definitive diagnostic test, but practical limitation its use The two basic methods for establishing a laboratory diagnosis of dengue infection are detection of the virus by culture and detection of anti-dengue antibodies (serology). Dengue virus can be isolated from human blood after mosquito inoculation, or from mosquito cell cultures. The virus is detected and identified by immunofluorescence using serotype-specific monoclonal antibodies (MAbs). Detection of dengue virus by culture is the definitive diagnostic test, but practical considerations limit its use. More commonly, a dengue infection is diagnosed by detection of anti-dengue immunoglobulin (Ig) M or IgG antibody in a patient's blood serum. A polymerase chain reaction (PCR) technique, studied by researchers from Japan and Thailand, provides a rapid, sensitive, and specific method to detect dengue virus. PCR allows simultaneous detection and serotyping of the virus in one procedure, using a pool of type-specific primer pairs for all four dengue virus serotypes. The references for the text are the Biological and Chemical Warfare Online Repository and Technical Holding System (BACWORTH), Version Battelle Memorial Institute, 1997, and Dengue haemorrhagic fever: diagnosis, treatment, prevention and control. 2nd edition.  Geneva : World Health Organization The reference for the images is 18 June 2001

18 Clinical spectrum There are actually four dengue clinical syndromes:
Undifferentiated fever; Classic dengue fever; Dengue hemorrhagic fever, or DHF; and Dengue shock syndrome, or DSS. Dengue shock syndrome is actually a severe form of DHF.

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20 Diagnostic criteria Clinical Definition for Dengue Fever :
Acute febrile viral disease frequently presenting with headaches, bone or joint pain, muscular pains, rash, and leucopenia Clinical Definition for Dengue Hemorrhagic Fever : Fever, or recent history of acute fever Hemorrhagic manifestations Low platelet count (100,000/mm3 or less) Objective evidence of “leaky capillaries”  elevated hematocrit (20% or more over baseline) low albumin pleural or other effusions

21 Diagnostic criteria Clinical Definition for Dengue Shock Syndrome :
4 criteria for DHF + evidence of circulatory failure manifested indirectly by all of the following: Rapid and weak pulse Narrow pulse pressure (< 20 mm Hg) OR hypotension for age Cold, clammy skin and altered mental status Frank shock is direct evidence of circulatory failure

22 Grades of DHF Grade 1 Fever and nonspecific constitutional symptoms
Positive tourniquet test is only hemorrhagic manifestation Grade 2 Grade 1 manifestations + spontaneous bleeding Grade 3 Signs of circulatory failure (rapid/weak pulse, narrow pulse pressure, hypotension, cold/clammy skin) Grade 4 Profound shock (undetectable pulse and BP)

23 Grades of DHF

24 Hemorrhagic Manifestations of Dengue
Skin hemorrhages: petechiae, purpura, ecchymoses Gingival bleeding Nasal bleeding Gastrointestinal bleeding: Hematemesis, melena, hematochezia Hematuria Increased menstrual flow

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26 Red flag in DHF Danger Signs in Dengue Hemorrhagic Fever ;
Abdominal pain - intense and sustained Persistent vomiting Abrupt change from fever to hypothermia, with sweating and prostration Restlessness or somnolence Signs of impending shock and should alert clinicians that the patient needs close observation and fluids.

27 Treatment Supportive care Keep patient hydrated to prevent shock
24 April 2017 Treatment Supportive care Keep patient hydrated to prevent shock Hospitalization of patients with advanced symptoms Symptomatic treatment : antipyretic For complete treatment protocol refer to the following reference: Dengue hemorrhagic fever: diagnosis, treatment, prevention and control. World Health Organization. 2006 Treatment for classic dengue fever is supportive. Lost plasma should be replaced early with an electrolyte solution, plasma, or plasma expanders to prevent or treat reduced blood volume (hypovolemic) shock. Patients with mild dengue hemorrhagic fever can usually be rehydrated orally. In addition, an antipyretic drug can be used. Salicylates should be avoided. Patients with advanced symptoms should be hospitalized and treated with intravenous fluid therapy. Blood transfusions are contraindicated in persons with severe plasma leakage. The references for the text are the Biological and Chemical Warfare Online Repository and Technical Holding System (BACWORTH), Version Battelle Memorial Institute, 1997, and Dengue haemorrhagic fever: diagnosis, treatment, prevention and control. 2nd edition.  Geneva : World Health Organization 18 June 2001

28 Fluid replacement

29 Shock Management in Dengue

30 HIV / AIDS Gatot Sugiharto, MD, Internist Internal Medicine Department
Faculty of Medicine, Wijaya Kusuma University Surabaya GSH - Tropmed

31 INTRODUCTION(1) Human Immunodeficiency Virus
H = Infects only Human beings I = Immunodeficiency virus weakens the immune system and increases the risk of infection V = Virus that attacks the body Acquired Immune Deficiency Syndrome A = Acquired, not inherited I = Weakens the Immune system D = Creates a Deficiency of CD4+ cells in the immune system S = Syndrome, or a group of illnesses taking place at the same time DR. S.K CHATURVEDI

32 INTRODUCTION(2) The HIV : virus that causes AIDS.
HIV attacks the immune system by destroying CD4 positive (CD4+) T cells, a type of white blood cell that is vital to fighting off infection  vulnerable to other infections, diseases and other complications. AIDS is the final stage of HIV infection. AIDS is diagnosed when someone has one or more opportunistic infections, such as pneumonia or tuberculosis, and has a dangerously low number of CD4+ T cells (less than 200 cells/cmm blood).

33 HIV Class of viruses : retroviruses, RNA virus
HIV uses an enzyme called reverse transcriptase to convert its RNA into DNA (deoxyribonucleic acid) and then proceeds to replicate itself using the cell's machinery. HIV belongs to a subgroup lentiviruses, or "slow" viruses  having a long time period between initial infection and beginning of serious symptoms  unaware of HIV infection, can spread the virus to others. Similar versions of HIV : feline immunodeficiency virus (FIV) in cats and simian immunodeficiency virus (SIV) in monkeys and other nonhuman primates.

34 PMTCT Policy for Barbados - Dr. Anton Best, MOH

35 PMTCT Policy for Barbados - Dr. Anton Best, MOH

36 HIV structure

37 HIV/AIDS transmission
Sexual transmission Heterosexual Homosexual Blood and blood products IV drug use Transfusions Haemophilia Other (knives, needle) Vertical transmission During pregnancy During birth Breastfeeding

38 HIV is not transmitted by
Coughing, sneezing Insect bites Touching, hugging Water, food Kissing Public baths Handshakes Work or school contact Using telephones Sharing cups, glasses, plates, or other utensils DR. S.K CHATURVEDI

39 Pathogenesis HIV destroys CD4 positive (CD4+) T cells, which are crucial for the human immune system. less equipped to fight off infection and disease  resulting in the development of AIDS. Most people who are infected can carry the virus for years before developing any serious symptoms until the number of CD4+ T cells decline Antiretroviral help reduce the amount of virus in the body, preserve CD4+ T cells and dramatically slow the destruction of the immune system.

40 Generally people in good health have roughly 800 to 1,200 CD4+ T cells per cmm of blood.
Some people who have been diagnosed with AIDS have fewer than 50 CD4+ T cells in their entire body.

41 HIV Replication Cycle

42 Steps in the HIV Replication Cycle
Fusion of the HIV cell to the host cell surface. HIV RNA, reverse transcriptase, integrase, and other viral proteins enter the host cell. Viral DNA is formed by reverse transcription. Viral DNA is transported across the nucleus and integrates into the host DNA. New viral RNA is used as genomic RNA and to make viral proteins. New viral RNA and proteins move to cell surface and a new, immature, HIV virus forms. The virus matures by protease releasing individual HIV proteins.

43 Progression of HIV Infection
Progression of HIV disease is measured by: CD4+ count Degree of immune suppression Lower CD4+ count means decreasing immunity Viral load Amount of virus in the blood Higher viral load means more immune suppression DR. S.K CHATURVEDI

44 Clinical Progression of HIV
Acute Primary Infection Once HIV enters the body, the virus infects a large number of CD4+ T cells and replicates rapidly. During this acute phase of infection, the blood has a high number of HIV copies (viral load) that spread throughout the body, seeding in various organs, particularly the lymphoid organs such as the thymus, spleen, and lymph nodes. During this phase, the virus may integrate and hide in the cell’s genetic material. Shielded from the immune system, the virus lies dormant for an extended period of time In the acute phase of infection, up to 70 percent of HIV-infected people suffer flu-like symptoms.

45 The Immune System Strikes Back
Two to four weeks after exposure to the virus, the immune system fights back with killer T cells (CD8+ T cells) and B-cell- produced antibodies. HIV levels in the blood are dramatically reduced. At the same time, CD4+ T cell counts rebound and for some individuals, the number rises to its original level. Clinical Latency During this phase, a person infected with HIV may remain free of HIV-related symptoms for several years despite the fact that HIV continues to replicate in the lymphoid organs where it initially seeded

46 Progression to AIDS The immune system eventually deteriorates to the point that the human body is unable to fight off other infections. The HIV viral load in the blood dramatically increases while the number of CD4+ T cells drops to dangerously low levels HIV-infected person is diagnosed with AIDS when he or she has one or more opportunistic infections, such as pneumonia or tuberculosis, and has fewer than 200 CD4+ T cells per cubic millimeter of blood.

47 Natural History of HIV Infection

48 Natural History of HIV Infection
DR. S.K CHATURVEDI

49 Early symptoms In the initial stages of HIV infection, most people will have very few, if any, symptoms. Within a month or two after infection, individuals may experience a flu-like illness, including: Fever, headache , tiredness Enlarged lymph nodes in the neck and groin area These symptoms usually disappear within a week to a month and are often mistaken for another viral infection, such as influenza (flu). However, during this period people are highly infectious because HIV is present in large quantities in genital fluids and blood. Some people infected with HIV may experience more severe symptoms initially or a longer duration of clinical symptom , while others may remain symptom-free for 10 years or more.

50 Later Symptoms Rapid weight loss
Recurring fever or profuse night sweats Extreme and unexplained fatigue Prolonged swelling of the lymph glands in the armpits, groin or neck Diarrhea that lasts for more than a week Sores of the mouth, anus or genitals Pneumonia Red, brown, pink or purplish blotches on or under the skin or inside the mouth, nose or eyelids Memory loss, depression and other neurological disorders. Each of these symptoms can be related to other illnesses. The only way to determine if you are infected with HIV is to get tested.

51 Virus can be transmitted during each stage
HIV spectrum Virus can be transmitted during each stage Seroconversion : Infection with HIV, antibodies develop Asymptomatic : No signs of HIV, immune system controls virus production Symptomatic : Physical signs of HIV infection, some immune suppression AIDS : Opportunistic infections, end-stage disease DR. S.K CHATURVEDI

52 ABC Approach The ABC Approach to prevent sexual transmission of HIV
Abstain Be faithful Use a Condom Limits of the ABC-Approach Lack of resources Gender inequality Faithfulness of partners

53 Types of HIV Tests Healthcare providers can test a sample of blood to see if it contains human antibodies (disease-fighting proteins) specific to HIV. The two key types of HIV antibody tests are the enzyme-linked immunosorbent assay (ELISA) and the Western blot. However, these antibody tests may not detect HIV antibodies in someone who has been recently infected with HIV (within one to three months of infection). In these situations, healthcare providers can test the blood for the presence of HIV genetic material. This test is extremely critical for identifying recently infected individuals who are at risk for unknowingly infecting others with HIV.

54 Voluntary Counselling and Testing (VCT)
Why should I get tested? How does the test work? Where to get tested? Voluntary testing vs. Mandatory testing Confidential testing and Anonymous testing Home sampling and testing

55 Treatment Antiretroviral drugs (ARVs) Are not a cure
Slow down the process of replication of HIV in the human body Prevent and treat Opportunistic Infections Prevent mother-to-child-transmission • During pregnancy and delivery • Safer infant feeding Access to services / availability of drugs Availability, Coverage, Impact

56 Treatment Important role of institutions (hospitals, clinics, VCT centres) Conditions to support treatment Medication adherence plan Living positively • Adopt a healthy diet • Exercise regularly • Avoid alcohol and tobacco, or certainly minimize their consumption • Reduce stress • Avoid all forms of infection (when possible) because they may compromise your health and further weaken one’s immune system • Don’t use drugs other than those prescribed by your doctor • Visit the doctor regularly

57 Treatment of HIV Infection
Today, there are 31 antiretroviral drugs (ARVs) approved by the U.S. Food and Drug Administration (FDA) to treat HIV infection. These treatments do not cure people of HIV or AIDS. Rather, they suppress the virus, even to undetectable levels, but they do not completely eliminate HIV from the body By suppressing the amount of virus in the body, people infected with HIV can now lead longer and healthier lives. However, they can still transmit the virus and must continuously take antiretroviral drugs in order to maintain their health quality.

58 Post Exposure Prophylaxis (PEP) for Healthcare Workers
Intact skin, mouth or nose: immediately wash with soap and water and rinse thoroughly to remove all potentially infectious particles. Cut or punctured skin: allow to bleed fully. Eye: flush immediately with water, then irrigate with normal saline for 30 minutes. Consider post exposure prophylaxis (PEP) if high risk of transmission: 4 week course of zidovudine (ZDV) preferable to start within 1-2 hours The US Centers for Disease Control considers exposure to be high risk if the injury to the healthcare worker is deep, there is visible blood on the device causing injury, the injury was caused by a device previously placed in the client’s vein or artery, or the source patient died as a result of AIDS within 60 days of exposure. Before initiating treatment with antiviral agents, the individual should know that knowledge about the efficacy and toxicity of treatment and potential side effects of treatment is limited. Source: CDC 1996.

59 Post Exposure Treatment of Healthcare Workers, continued
HIV testing immediately, 6 weeks, 6 months and 12 months Treatment, if started, should continue for 4 weeks. Any or all drugs may be declined by exposed worker. For lesser exposures, prophylaxis is not recommended.

60 Prevention Currently, there is no vaccine to prevent HIV infection nor is there a cure for HIV/AIDS. To reduce risk of becoming infected with HIV or transmitting the virus to others: Consistent use of male latex condoms can help protect against HIV infection. Get tested regularly for HIV Practice abstinence Remain faithful to your spouse or partner Consistently use male latex or female polyurethane condoms Do not share needles


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