STUDY GUIDE
INFECTION &
INFECTIOUS DISEASES
PROGRAM STUDI PENDIDIKAN DOKTER
FAKULTAS KEDOKTERAN
CONTENTS
Table of contents ………..………. 1
Introduction ………. 2
Curriculum ……… 4
The Seven General Core Competencies………. 6
Block Team ………... 7
Facilitators ……… 8
Time Table Regular Class ……… 9
Time Table English Class ……….. 9
Student’s Project……….. 14
Assessment method ………... 16
Learning Program ……….. 17
Lecture ………. 17
Learning Task and Self Assessment……….17
Curriculum Mapping ………... 60
INTRODUCTION
Due to the application of integrated curriculum at the Faculty of Medicine Udayana University, the discipline-based subjects of the previous curriculum such as Biology, Anatomy, Physiology, Internal Medicine, etc have been integrated and incorporated into several blocks. One of these blocks is Infections and Infectious Diseases. In this block will be explained in general about pathogenesis, pathophysiology, sign, symptoms, clinical features, diagnosis, and management of certain infectious diseases commonly occur in community.
This book aims to give general information for medical students about infections and infectious diseases and important for facilitators and resource person while facilitating or guiding the students in learning process. This study guide consists of general information on learning time table, block team members, facilitators, and the core curriculum including learning outcomes, learning situations, learning tasks and self-evaluation items.
The block Infection and Infectious Diseases has the equivalent of 3 (three) credits. As a block of six credits, the learning processes will be carried out for 38 days starts from October, 6th 2017 as shown in the Time Table. Evaluation for infection and infectious disease will be held on 9th November 2017. Final mark of this block is combination between result of basic and clinical examination. During the 38 days of learning activities, the students will discuss several topics in varied forms of learning situations such as independent learning, small group discussion, lecture, and skill lab.
More than half of the learning material must be learned independently and in small group discussions. A lecture is given only to emphasize crucial things or objectivesof material and to prepare the students before discussion. For small group discussion, the students will be given learning tasks to solve and discuss. After discussion, students also have to evaluate their learning progress independently (self assessment).
From this block, we hope every medical student have knowledge and skill to diagnose and manage infections and certain infectious diseases commonly occur in community, as a frontline in community health.
Since the integrated curriculum of the Faculty of Medicine Udayana University is still in progress, this Study Guide will also, naturally, have some revisions in the future. Therefore, we kindly invite readers to give any comments or suggestions for its improvement and development.
CURRICULUM OF THE BLOCK
AIMS
To comprehend the biology of the infectious diseases
To apply and interpret common laboratory diagnosis of infectious diseases
To diagnose and manage common infectious diseases
To carry out basic immunization in children
LEARNING OUTCOMES
Comprehend the practical and clinical implications of the biology of infection
Apply the general principles of approach to patients with infectious diseases
Apply and interpret common laboratory diagnosis of common infectious diseases
Apply the basic principles of immunization in children
Diagnose and manage common bacterial infections (common Gram positive and negative, spirochetal)
Diagnose and manage common parasitic infections (common nematode, trematode, cestode, and protozoal infections)
Diagnose and manage common fungal infections
Clinically diagnose and manage common viral infections (caused by common respiratory virus, herpesvirus, arbovirus)
Clinically diagnose and manage Infection in pregnancy (TORCH)
CURRICULUM CONTENT
1. The biology of infection: bacterial, viral, fungal and parasitic.
a. Principles of bacterial infections such as Staphylococci, Streptococci, Neisseria, Salmonella, Vibrio, anaerobic bacteria¸ Leptospira, Mycobacteria, Gram positive bacilli)
b. Principles of viral infections such as respiratory virus (influenza virus, mumps, measles), retrovirus (HIV), herpesvirus (HSV 1, HSV 2, VZV, arbovirus (dengue virus, Japanese B encephalitis virus).
c. Principles of fungal infections such as Candida, Pneumocytis jiroveci, Histoplasma, Cryptococcus
d. Principles of parasitic infections such as Plasmodium, Toxoplasma gondii, Entamoeba histolytica and soil transmitted helminthes.
2. General approach to the patients with infection such as: a. Clinical manifestations (local and systemic infections)
3. Management patients with infection such as:
a. Common bacterial infections such as bacterial meningitis, typhoid fever, diarrhea, endocarditis, diphtheria, tetanus, food poisoning, genital gonorrhoeae, non gonococcal urethritis, etc.
b. Common parasitic infections such as malaria, amoebiasis, toxoplasmosis. c. Common fungal infection such as dermatophytosis, systemic candidiasis,
histoplasmosis, cryptococcosis, pneumocytis jiroveci pneumonia.
d. Common viral infections such as mumps, measles, influenza (especially H5N1), SARS, varicella, herpes labialis, herpes genitalis, dengue fever, Japanese B encephalitis, and HIV.
4. Immunization in children.
The Seven General Core Competencies
1. Patient Care
Demonstrate capability to provide comprehensive patient care that is compassionate, appropriate, and effective for the management of health problems, promotion of health and prevention of disease in the primary health care settings.
2. Medical Knowledge Base
Mastery of a core medical knowledge which includes the biomedical sciences, behavioral sciences, epidemiology and statistics, clinical sciences, the social aspect of medicine and the principles of medical ethics
3. Clinical skill
Demonstrate capability to effectively apply clinical skills and interpret the findings in the investigation of the patients
4. Communication
Demonstrate capability to communicate effectively and interpersonally to establish rapport with the patient, family, community at large, and professional associates, that results in effective information exchange, the creation of a therapeutically and ethically sound relationship
5. Information Management
Demonstrate capability to manager information which includes information access, retrieval, interpretation, appraisal, and application to patience’s specific problem, and maintaining records of his or her proactive for analysis and improvement
6. Professionalism
Demonstrate a commitment to carrying out professional responsibilities and to personal probity, adherence to ethical principles, sensitivity to a diverse patient population and commitment to carrying out continual self-evaluation of his or her professional standard and competence
7. Community-based and health system-based practice
PLANNERS TEAM
No Name Departement Phone
1 Prof. Dr. dr. Tuti Parwati Merati, SpPD, KPTI-FINASIM (Tropical Disease)Internal Medicine 08123806626
2 dr. Made Susila Utama, SpPD-KPTI Internal Medicine
(Tropical Disease) 08123815025
3 dr. Ratih Karna, Sp.KK Dermatology &Venerology 081337808844
4 dr. Ni Putu Ekawati, M.repro, Sp.PA PhatologyAnatomy 08113803933
5 dr. I Gusti Ayu Harry Sundariyati, S.Ked DME 081805380277
LECTURER
NO NAME DEPT PHONE
1. Prof. Dr. dr. Tuti Parwati Merati,
SpPD, KPTI-FINASIM (Tropical Disease)Internal Medicine 08123806626 3. dr. Made Susila Utama, SpPD-KPTI Internal Medicine
(Tropical Disease) 08123815025
4. Dr. dr. Agus Somia, SpPD-KPTI Internal Medicine
(Tropical Disease)
08123989353
5. dr. AA Yuli Gayatri, SpPD-KPTI Internal Medicine
(Tropical Disease)
08123803985
6. dr. Ni Made Dewi Dian Sukmawati, Sp.PD
Internal Medicine (Tropical Disease)
081805656501
7. dr W. Gustawan,M.Sc., Sp.A Pediatri 08123848241
8. dr. Made Bagiada, Sp.PD-KP Pulmonology 08123607874
9.
Dr. dr. Wayan Sudhana, SpPD-KGH Internal Medicine(Nefrology) 08123914095 10.
Dr. dr. IB Fajar Manuaba, SpOG GynecologyObstetric & 081558101719
11. dr. Dwi Lingga Utama, Sp.A (K) Pediatric 081353002002
12. dr. Ni Made Susilawati, Sp.S (K) Neurology 08124690137
13. Prof. dr. Made Swastika Adiguna, Sp.KK
Dermato &
Venerology 08123828548
14. Dr. dr. A.A.G.P. Wiraguna, Sp.KK Dermato &
Venerology 081338645288
15. dr. Kadek Swastika, M.Kes Parasitology 08124649002
16. dr. Ni Nengah Dwi Fatmawati, Sp.MK,
FACILITATORS
(REGULAR CLASS)
No Name Group Departement Phone (3Venuerd floor)
1 Dr. dr. Ni Made Linawati, M.Si A1 Histology 081337222567 3rd floor: R.3.01
2 dr. I Gusti Ayu Harry Sundariyati,
S.Ked A2 DME 081805380277
3rd floor: R.3.02
3 dr. Yukhi Kurniawan, Sp.And A3 Andrology 08123473593 3rd floor:R.3.03
4 dr. Ni Nengah Dwi Fatmawati, Sp.MK, Ph.D A4 Microbiology 087862200814 3rd floor:R.3.04
5 dr. Prima Sanjiwani Saraswati Sudarsa, M.Biomed, SpKK A5 Dermatovenerology 08123818826 3rd floor:R.3.05
6 dr. Sri Yenni Trisnawati GS, M.Biomed, Sp.S A6 Neurology 081236223000 3rd floor:R.3.06
7 Prof. Dr.dr. I Putu Gede Adiatmika,
M.Kes A7 Physiology 08123811019
3rd floor: R.3.07
8 dr. I Kadek Swastika, M.Kes A8 Parasitology 08124649002 3rd floor:R.3.08
9 dr. I Wayan Surudarma, Msi A9 Biochemistry 081338486589 3rd floor: R.3.21 10 dr. Ni Made Ari Suryathi,
M.Biomed, Sp.M A10 Opthalmology 085253651928
3rd floor: R.3.22
FACILITATORS
(ENGLISH CLASS)
No Name Group Departement Phone Venue
(3rd floor)
1 dr. Putu Cintya D.Y, MPH B1 Public Health 081353380666 3rd floor:R.3.01
2 Dr. dr. I Dewa Made Sukrama, Msi,Sp.MK (K) B2 Microbiology 081338291965 3rd floor:R.3.02
3 dr. I Ketut Wibawa Nada, Sp.An B3 Anestesiology 087860602995 3rd floor:R.3.03
4 dr. Ni Putu Ekawati, M.Repro, Sp.PA B4 AnatomyPatology 08113803933 3rd floor:R.3.04
5 Dr. dr. Susy Purnawati, M.KK B5 Physiology 08123989891 3rd floor:R.3.05
6 Prof. dr. I G M. Aman, Sp.FK B6 Pharmacology 081338770650 3rd floor:R.3.06
7 dr. Ni Putu Witari, Sp.S B7 Neurology 081338724040 3rd floor: R.3.07
8 dr. I Wayan Sugiritama, M.Kes B8 Histology 08164732743 3rd floor:R.3.08
9 Dr. dr. I Made Muliarta, M.Kes B9 Physiology 081338505350 3rd floor:R.3.21
TIME-TABLE
(Block Infection and infectious Diseases)
DAY/DATE Time TOPIC Learning
Situation Place PIC Regular Class English Class 1 Friday Oct 6th 2017
09.00-09.30 08.00-08.30 Lecture 1: Introduction of block infection and
infectious disease
Introduction of block and
basic infection
Class room
Dr Made Susila Utama, SpPD-KPTI
09.30-10.00
08.30-09.00
Lecture 2: Malaria Lecture Class room
Dr Made Susila Utama, SpPD-KPTI 12.00-13.30 09.00-10.30 Individual learning 13.30-15.00 10.30-12.00 Small Group Discussion Disc. Room facilitator 10.00-11.30 12.30-14.00 Individual learning 15.00-15.30 14.00-14.30 Plenary session Class room 15.30-16.00 14.30-15.00 Plenary session Class room 2
Monday Oct 9th 2017
09.00-10.00
08.00-09.00
Lecture 3: Dengue viral infection
Lecture Class room
Dr Dewi Dian Sukmawati, SpPD 12.00-13.30 09.00-10.30 Individual learning 12.00-13.30 10.30-12.00 Small Group Discussion Disc. Room facilitator 13.30-15.00 12.30-14.00 Individual learning 15.00-16.00 14.00-15.00 Plenary Class room
Dr Dewi Dian Sukmawati, SpPD
3 Tuesday
Oct 10th 2017
09.00-10.00
08.00-09.00
Lecture 4: Host response to infection (viral, bacterial, fungal and parasite) Lecture Class room
15.00-16.00 14.00-15.00 Plenary Class room
Prof DR Dr Tuti Parwati Merati,
SpPD-KPTI
4 Wednesday
Oct 11th 2017
09.00-10.00
08.00-09.00
Lecture 5: Infection in Pediatric
Lecture Class room
Dr Dwi Lingga Utama, SpA (K)
12.00-13.30 09.00-10.30 Individual learning 13.30-15.00 10.30-12.00 Small Group Discussion Disc. room Facilitator 10.00-11.30 12.30-14.00 Individual learning 15.00-16.00 14.00-15.00 Plenary Class room
Dr Dwi Lingga Utama, SpA (K)
5 Thursday
Oct 12th 2017
09.00-10.00
08.00-09.00
Lecture 6: infection in pregnancy
Lecture Class room
DR Dr IB Fajar Manuaba, SpOG 12.00-13.30 09.00-10.30 Individual learning 13.30-15.00 10.30-12.00 Small Group Discussion Disc. room Facilitator 10.00-11.30 12.30-14.00 Individual learning Class room 15.00-16.00 14.00-15.00
Plenary DR Dr IB Fajar
Manuaba, SpOG
6 Friday Oct 13th
2017
09.00-10.00
08.00-09.00
Lecture 7: Central nervous system infection (meningitis, encephalitis) Lecture Class room
Dr Ni Made Susilawati, SpS(K) 12.00-13.30 09.00-10.30 Individual learning 13.30-15.00 10.30-12.00 Small Grup Discussion Disc. room Facilitator 10.00-11.30 12.30-14.00 Individual learning 15.00-16.00 14.00-15.00 Plenary Class room
Dr Ni Made Susilawati, SpS(K)
7 Monday Oct 16th 2017
09.00-09.30
08.00-08.30
Lecture 8: typhoid fever
Lecture Class room
DR Dr Ketut Agus Somia, SpPD-KPTI
09.30-10.00
08.30-09.00
Lecture 9: Acute gastroenteritis
Lecture Class room
15.00-15.30 14.00-14.30 Plenary Class room
DR Dr Ketut Agus Somia, SpPD-KPTI
15.30-16.00
14.30-15.00
Plenary Dr AAA Yuli
Gayatri, SpPD-KPTI
8 Tuesday
Oct 17th 2017 09.00-10.00 08.00-09.00 Lecture 10:HIV infection: pathogenesis and opportunistic infections Lecture Class room
Prof DR Dr Tuti Parwati Merati, SpPD-KPTI 12.00-13.30 09.00-10.30 Individual learning 13.30-15.00 10.30-12.00 Small Group Discussion Disc. room Facilitator 10.00-11.30 12.30-14.00 Individual learning 15.00-16.00 14.00-15.00 Plenary Class room
Prof DR Dr Tuti Parwati Merati,
SpPD-KPTI
9 Wednesday
Oct 18th 2017 09.00-09.30 08.00-08.30 Lecture 11: Leptospirosis Lecture Class room
DR Dr Ketut Agus Somia, SpPD-KPTI 09.30-10.00 08.30-09.00 Lecture 12: Filariasis
Lecture Dr Dewi Dian
Sukmawati, SpPD 12.00-13.30 09.00-10.30 Individual learning 13.30-15.00 10.30-12.00 Small Group Discussion Disc. room Facilitator 10.00-11.30 12.30-14.00 Individual learning 15.00-15.30 14.00-14.30 Plenary Class room
DR Dr Ketut Agus Somia, SpPD-KPTI 15.30-16.00 14.30-15.00 Plenary Class room
Dr Dewi Dian Sukmawati, SpPD
10 Thursday
Oct 19th 2017
09.00-09.30
08.00-08.30
Lecture 13: Child Imunization Lecture Class room Dr Wayan Gustawan, SpA(K) 09.30-10.00 08.30-09.00 Lecture 14: Bacteriemia, sepsis Lecture Class room
15.30-16.00 14.30-15.00 Plenary Class room
Dr Made Susila Utama, SpPD-KPTI
11 Friday Oct 20th
2017
09.00-09.30
08.00-08.30
Lecture 15: urinary tract infection
(acute pyelonephritis, lower urinary tract
infection)
Lecture Class room
DR Dr Wayan Sudhana, SpPD-KGH 09.30-10.00 08.30-09.00
Lecture 16: Lower respiratory tract infection (pneumonia, acute bronchitis) Lecture Class room
Dr Made Bagiada, SpPD-KP 12.00-13.30 09.00-10.30 Individual learning 13.30-15.00 10.30-12.00 Small group discussion Disc. room Facilitator
10.00-11.30 12.30-14.00 Individuallearning 15.00-15.30 14.00-14.30 Plenary Class room
DR Dr Wayan Sudhana,
SpPD-KGH
15.30-16.00 14.30-15.00 Plenary Classroom Dr Made Bagiada,SpPD-KP
12 Monday
Oct 23rd 2017
09.00-09.30
08.00-08.30
Lecture 17: avian influenza, SARS
Lecture Class room
DR Dr Ketut Agus Somia, SpPD-KPTI
09.30-10.00
08.30-09.00
Lecture 18: tetanus Lecture Dr AAA Yuli Gayatri, SpPD-KPTI 12.00-13.30 09.00-10.30 Individual learning 13.30-15.00 10.30-12.00 Small Group Discussion Disc. room Facilitator 10.00-11.30 12.30-14.00 Individual learning 15.00-15.30 14.00-14.30 Plenary Class room
DR Dr Ketut Agus Somia, SpPD-KPTI 15.30-16.00 14.30-15.00 Plenary Class room
Dr AAA Yuli Gayatri, SpPD-KPTI
13 Tuesday
Oct 24th 2017
09.00-10.00
08.00-09.00
Lecture 19: Skin infection
Lecture Class
room Prof. dr. Made Swastika Adiguna,
10.00-11.30 12.30-14.00 Individual learning 15.00-16.00 14.00-15.00 Plenary Class room
Prof. dr. Made Swastika Adiguna, Sp.KK
14 Wednesday
Oct 25th 2017
09.00-10.00
08.00-09.00
Lecture 20: S Sexually Transmitted
Infection
Lecture Class room
Dr. dr. A.A.G.P. Wiraguna, Sp.KK 12.00-13.30 09.00-10.30 Individual learning 13.30-15.00 10.30-12.00 Small Group Discussion Disc. room 10.00-11.30 12.30-14.00 Individual learning 15.00-16.00 14.00-15.00 Plenary Class room 15 Thursday Oct 26th
2017 08.00-16.00 08.00-16.00 STUDENT PROJECT (REGULAR CLASS) Theat er room /Class room Evaluator/ facilitator 16 Friday Oct 27th
2017 08.00-16.00 08.00-16.00 STUDENT PROJECT (ENGLISH CLASS) Theat er room /Class room Evaluator/ facilitator 17 Monday Oct 30th 2017
09.00-16.00
08.00-15.00
Basic Clinical skill : Diagnostic of Dengue Viral
Infection
Skill Lab
dr. Ni Made Dewi Dian Sukmawati, Sp.PD
Vaccine Administration Skill Lab
dr W. Gustawan,M.Sc.,
Sp.A
18 Friday Nov 3rd 2017
09.00-16.00
08.00-15.00
Basic Clinical skill : Culture sampling technique in
gynecology
Skill Lab
DR Dr IB Fajar Manuaba, SpOG
19 Monday Nov 6th 2017
09.00-16.00
08.00-15.00
Basic Clinical skill : Fecal Examination
dr. Kadek Swastika, M.Kes
20 Tuesday Nov 7th 2017
09.00-16.00
08.00-15.00
Basic Clinical skill : dr. Ni Nengah Dwi Fatmawati, Sp.MK,
Ph.D
Wednesday Nov 08th
2017
PRE-EVALUATION BREAK
Thursday Nov 09th
STUDENT PROJECT
Regulation:
TITLE Name: NIM:
Faculty of Medicine, Udayana University 2016
1. Introduction (Pendahuluan)
2. Content (Isi sesuai dengan judul paper) 3. Summary (Ringkasan)
4. References (Daftar pustaka): Vancouver style 5. Pages: 6-10, Spasi: 1.5, Time New Roman:12
TOPIC Regular Class (Class A)
GROUP DATE &
TIME
TITLE PEMBIMBING/
FASILITATOR
EVALUATOR
1 Tuesday,
Sept 20th
2016,
08.30-09.00
Cerebral abses dr. Ni Made
Susilawathi, Sp.S (K)
2 09.00-09.30 Cerebral
toxoplasmosis
3 09.30-10.00 Multi drug
resisten (MDR) TB
dr. Made Bagiada, Sp.PD-KP
4 10.00-10.30 Spondilitis TB
5 10.30-11.00 Acute infection
pancreatitis dr. A.A.A. Yuli Gayatri,
Sp.PD-KPTI
6 11.00-11.30 Pes
11.30-12.30 BREAK
7 12.30-13.00 Leishmaniasis dr. Dewi Dian
Sukmawati, Sp.PD
8 13.00-13.30 Tripanosomiasis
9 13.30-14.00 Cytomegalovirus
infection
Dr. dr. Ketut Agus Somia, Sp.PD-KPTI
10 14.00-14.30 Squamous cell
carcinoma
TOPIC
English Class (Class B)GROUP DATE & TIME TITLE PEMBIMBING/
FASILITATOR
EVALUATOR
1 Wednesday,
Oct 5th 2016,
08.30-09.00
Nasopharyngeal carcinoma
(associated with EBV infection)
dr. Wayan Gustawan, Sp.A (K)
2 09.00-09.30 Hairy leukoplakia
(associated with EBV infection)
3 09.30-10.00 Korioretinitis dr. Ratih
Karna, Sp.KK
4 10.00-10.30 Carcinoma servik
(associated with HPV infection)
5 10.30-11.00 Penyakit jantung
rematik
dr. Dwi Lingga Utama, Sp.A (K)
6 11.00-11.30 Endoftalmitis
11.30-12.30 BREAK
7 12.30-13.00 Hepatitis C dr. Made
Susila Utama, Sp.PD-KPTI
8 13.00-13.30 Abses payudara
9 13.30-14.00 Epididimitis Dr. dr. I.B.
Fajar Manuaba, Sp.OG
ASSESSMENT METHOD
1. Assessment will be held twice, for infection & infectious diseases. Final mark is combination beteween this mark. The time provision is 100 minutes. The number of MCQ is 100 with passing point 70.
2. Assessment in this block consists of:
SGD : 5%
Student Project (Paper) : 10%
LEARNING PROGRAM
Lecture 1
INTRODUCTION OF BLOCK INFECTION AND INFECTIOUS
DISEASE
Abstract
Infections and infectious diseases are a great burden on many societies, including Indonesia. To reduce that burden an integrated approach is required, combining health promotion, disease prevention and patient treatment. The prerequisite for success in this fight is the participation of all health care professionals. Should know and understand terminology commonly use in the context of infectious disease. Infectious diseases are disorders or diseases caused by organisms — such as bacteria, viruses, fungi or parasites. Many organisms live in and on our bodies. They're normally harmless or even helpful, which we called them normal flora; but under certain conditions, some organisms may cause disease. This organisms called as pathogen as they can produced pathology to the body.
Infectious diseases are one of the leading causes of death worldwide. Infectious diseases can be spread directly or indirectly. Some infectious diseases can be passed from person to person. Some are transmitted by bites from insects or animals. And others are acquired by ingesting contaminated food or water or being exposed to organisms in the environment.
Many infectious diseases become difficult to control if the infectious agents evolve resistance to commonly used drugs: For example, bacteria can accumulate mutations in their DNA or acquire new genes that allow them to survive contact with antibiotic drugs that would normally kill them.
Signs and symptoms vary depending on the organism causing the infection, but often include fever and fatigue. Mild infections may respond to rest and home remedies, while some life-threatening infections may require hospitalization.
Many infectious diseases, such as measles and chickenpox, can be prevented by vaccines but many other still do not have vaccine available. Other prevention mean such as frequent and thorough hand-washing helps protect from most infectious diseases.
Symptoms
Each infectious disease has its own specific signs and symptoms. General signs and symptoms common to a number of infectious diseases include: fever, fatigue, muscle aches, coughing and diarrhea
Transmission: an infection can be spread through direct and indirect contact Direct contact
An easy way to catch most infectious diseases is by coming in contact with a person or animal who has the infection. Three ways infectious diseases can be spread through direct contact are:
Person to person. A common way for infectious diseases to spread is through the
the exchange of body fluids from sexual contact. The person who passes the germ may have no symptoms of the disease, but may simply be a carrier.
Animal to person. Being bitten or scratched by an infected animal — even a pet —
can make you sick and, in extreme circumstances, can be fatal. Handling animal waste can be hazardous, too. For example, you can acquire a toxoplasmosis infection by scooping your cat's litter box.
Mother to unborn baby. A pregnant woman may pass germs that cause infectious
diseases to her unborn baby. Some germs can pass through the placenta. Germs in the vagina can be transmitted to the baby during birth.
Indirect contact
Touching: Disease-causing organisms also can be passed by indirect contact.
Many germs can linger on an inanimate object, such as a tabletop, doorknob or faucet handle. When you touch a doorknob handled by someone ill with the flu or a cold, for example, you can pick up the germs he or she left behind. If you then touch your eyes, mouth or nose before washing your hands, you may become infected.
Vectors/insect bites - Some germs rely on insect carriers — such as mosquitoes,
fleas, lice or ticks — to move from host to host. These carriers are known as vectors. Mosquitoes can carry the malaria parasite or West Nile virus, and deer ticks may carry the bacterium that causes Lyme disease.
Food/water contamination : disease-causing germs can infect you is through
contaminated food and water. This mechanism of transmission allows germs to be spread to many people through a single source. E. coli, for example, is a bacterium present in or on certain foods — such as undercooked hamburger or unpasteurized fruit juice.
Risk factors
Anyone can catch infectious diseases easier than other people because the body immune system is not work well. This may occur if there are primary or secondary immune deficiency , such as : Taking steroids or other medications that suppress immune system, such as anti-rejection drugs for a transplanted organ, certain types of cancer or other disorders that affect the immune system, infection by HIV or AIDS. In addition, certain other medical conditions may predispose you to infection, including implanted medical devices, malnutrition and extremes of age, among others.
Complications
Most infectious diseases have only minor complications. But some infections — such as pneumonia, AIDS and meningitis — can become life-threatening. A few types of infections have been linked to a long-term increased risk of cancer: hepatitis B and C have been linked to liver cancer, human papillomavirus is linked to cervical cancer, Helicobacter pylori is linked to stomach cancer and peptic ulcers and In addition, some infectious diseases may become silent, only to appear again in the future — sometimes even decades later. For example, someone who's had a chickenpox infection may develop shingles much later in life.
Diagnosis
Diagnosis can be made with clinical symptoms and signs. Because many of infectious disease have a very similar symptoms and signs, usually laboratory or imaging test would be needed to confirmed the diagnosis
Many infectious diseases have similar signs and symptoms. Samples of body fluids can sometimes reveal evidence of the particular microbe that's causing illness. Samples can get from blood, urine, throat swabs, stool sample, spinal tap (lumbar puncture). A technician obtains a sample with a standard procedure from each.
Imaging scans
Imaging procedures — such as X-rays, computerized tomography and magnetic resonance imaging — can help pinpoint diagnoses and rule out other conditions that may be causing the symptoms.
Biopsies
During a biopsy, a tiny sample of tissue is taken from an internal organ for testing. For example, a biopsy of lung tissue can be checked for a variety of fungi that can cause a type of pneumonia.
Treatment
Knowing what type of germ is causing the illness makes it easier to choose appropriate treatment such as : antibiotics, anti viral, anti fungal, and anti-parasitics.
However, the use of those agents should be use appropriately. The overuse of antibiotics has resulted in several types of bacteria developing resistance to one or more varieties of antibiotics. This makes these bacteria much more difficult to treat As an alternative medicine, a number of products have been purported to help fend off common illnesses, such as the cold or flu. Cranberry, echinacea, garlic, ginseng, vitamin C, D and zinc are among other. While some of these substances have appeared promising in early trials, follow-up studies may have had negative or inconclusive results. More research needs to be done.
Prevention
Infectious diseases can be prevented by vaccines but many other still do not have vaccine available. Prevention to infectious disease transmission with no vaccine available should use another approach. Personal protected equipment such as gown, masker, google, gloves, and shoes boot. Infectious disease transmitted by vectors should avoid to being bitten by mosquitoes or other insects may be useful, such as wearing long sleeve shirt, and putting mosquitos repellent. Other prevention means such as frequent and thorough hand-washing helps protect from most infectious diseases.
Learning tasks:
1. How do we know that a patient in our hospital is suffering from a kind of infectious disease?
2. How he or she can get it?
3. What prevention do we need to do to avoid of getting any infectious diseases?
Self assessment:
1. Describe all common terminology use in the context of infectious diseases. 2. Describe general clinical manifestation of infectious diseases.
Lecture 2
MALARIA
Abstract
Malaria is caused by infection of red blood cells with protozoan parasites of the genus Plasmodium inoculated into the human host by a feeding female anopheline mosquito. The five human Plasmodium species transmitted from person to person are P. falciparum, P. vivax, P. Ovale (two species), P. Malariae and P. Knowlesi. The first symptoms of malaria are nonspecific and similar to those of a minor systemic viral illness. They comprise headache, lassitude, fatigue, abdominal discomfort and muscle and joint aches, usually followed by fever, chills, perspiration, anorexia, vomiting and worsening malaise. Disease progression to severe malaria may take days but can occur within a few hours. Severe malaria usually manifests with one or more of the following: coma (cerebral malaria), metabolic acidosis, severe anaemia, hypoglycaemia, acute renal failure or acute pulmonary oedema. If left untreated, severe malaria is fatal in the majority of cases. All patients with suspected malaria should be treated on the basis of a confirmed diagnosis by microscopy examination or RDT testing of a blood sample. Management of uncomplicated malaria using ACT (Artemisinine Combination Therapy) for 3 days but severe malaria must treated with anti malaria intravenous (artesunate).
Learning task
1. Explain clinical symptom and sign of malaria
2. Differentiate between uncomplicated malaria and severe malaria 3. Management uncomplicated malaria and severe malaria
Self assessment Case:
1. Male, 23 years old come to internal medicine clinic with fever for 6 days. Fever was intermittenly every 2 days, fever was followed by chills and sweathing. He has history travel to Papua.
- How to make diagnosis in this case? - How to manage this case?
2. Female, 34 years old come to emergency room with severe headache and fever for 4 days. Physical examination: icterus +, lien S2. Lab examination Hb 4 g/dL, bil total 4,3 mg/dL and plasmodium falciparum on smear.
Lecture 3
DENGUE FEVER, DENGUE HEMORRHAGIC FEVER, DENGUE
SHOCK SYNDROME
ABSTRACT
Dengue is mosquito borne viral infection, which causing acute fever and occasionally develops into potential lethal complication. Dengue virus is transmitted by female mosquitoes mainly of the species Aedes aegypti and, to a lesser extent, Ae. albopictus. This mosquito also transmits Chikungunya, Yellow Fever and Zika infection. About half of world’ population were at risk, Dengue is widespread throughout the tropics, with local variations in risk influenced by rainfall, temperature and unplanned rapid urbanization.
There are 4 distinct, but closely related, serotypes of the virus that can cause dengue (DEN-1, DEN-2, DEN-3 and DEN-4). Recovery from infection by one provides lifelong immunity against the particular serotype with partial and temporary cross-immunity to the other serotypes after recovery. Subsequent infections by other serotypes increase the risk of developing severe dengue.
Dengue should be suspected when a high fever is present, accompanied by 2 of the following symptoms: severe headache, pain behind the eyes, muscle and joint pains, nausea, vomiting, swollen glands or rash. Symptoms usually last for 2–7 days, after an incubation period of 4 – 5 days (range 3 – 14 days) after the bite from an infected mosquito. Severe dengue is a potentially deadly complication due to plasma leakage, fluid accumulation, respiratory distress, severe bleeding, or organ impairment. Warning signs occur 3–7 days after the first symptoms in conjunction with a decrease in temperature and include: severe abdominal pain, persistent vomiting, and rapid breathing, bleeding gums, fatigue, restlessness and blood in vomit. The next 24–48 hours of the critical stage can be lethal; proper medical care is needed to avoid complications and risk of death.
For the purpose of clinical management, WHO classifies dengue illness as (i) dengue with or without warning signs for progression towards severe dengue and (ii) severe dengue. Warning signs of severe dengue include abdominal pain or tenderness, persistent vomiting, clinical fluid accumulation, mucosal bleeding, lethargy or restlessness, liver enlargement of >2 cm, or an increase in Hematocrit concurrent with a rapid decrease in platelet count. Criteria for severe dengue include any sign of severe plasma leakage leading to shock or fluid accumulation with respiratory distress, severe bleeding, or severe organ impairment.
There is no specific treatment for dengue, maintenance of the patient’s body fluid volume is critical in management of severe dengue. Vaccine for prevention is now commercially available, Dengvaxia (CYD – TDV) for use in individual age 9 – 45 years living in area with high burden of disease.
LEARNING TASK
Case 1:
IMD, 16 year old male student come to a private clinic with acute onset of high fever. The fever starts abruptly one day before accompanied by nausea and retro orbital pain.
1. What other information needed in anamnesis of this patient? What data should be obtained during physical examination?
2. The evaluation shows vital sign was stabile without any sign of bleeding, the patient able to drink plenty and eat normally. What is the diagnosis of this patient? How about further plan for this case, including planning for diagnostic, treatment, monitoring and patient and family’s education?
3. The next day, he showed his laboratory evaluation. WBC: 1.03 x 103/uL. Hb. 17 g/dL. HCT 54 %. Plt. 98 x 103/uL. What is the diagnosis of this patient? How about further plan for this case, including planning for diagnostic, treatment, monitoring and patient and family’s education?
Case 2:
25 year old woman, working as a private secretary, come to the clinic with 4 days of fever. Since morning she also had her menstrual bleeding which comes 2 weeks early. The initial evaluation revealed moderately ill, fully alert. Blood pressure 90/76 mmHg. Pulse rate 124 x/minutes. Respiratory rate: 22 x/minutes. Temperature axillae: 36.7˚C. Hepatomegaly 3 cm below costal arch, tender on palpation, the acrals were cold. She has her laboratory evaluation: WBC: 3.02 x 103/uL; Hb. 16 g/dL. HCT: 51.2 %. Plt.32 x 103/uL
1. What is the diagnosis of this patient? How about further plan for this case, including planning for diagnostic, treatment, monitoring and patient and family’s education?
2. Is there any indication for platelet transfusion in this case? Why?
3. The patient was then hospitalized, by the third day of her hospital stay, she complain about shortness of breath and cough if she change position from supine to sitting. The physical evaluation revealed dullness on lower part of right hemithorax with decreased breath sounds. What kind of complication can be expected in severe dengue cases? How can we establish the diagnosis?
Self assessment
1. How can we differentiate between dengue fever and dengue hemorrhagic fever? Make a comparison chart on this issue!
2. Both DHF grade 3 and 4 are included as DSS. How can we differentiate between the two of them?
3. What is NS1 dengue antigen? When is the best way to use it?
4. How about dengue serology? When IgM anti-Dengue become positive? When the Ig G anti-dengue become positive? Make the chart on the possible result and its interpretation!
REFERENCES:
1. World Health Organization. Dengue Guidelines for Diagnosis, Treatment, Prevention and Control. Geneva, Switzerland: 2009. Available at
http://www.who.int/tdr/ publications/documents/dengue-diagnosis.pdf
2. Messina JP, et al. Global spread of dengue virus types: mapping the 70 year history. Trends Microbiol. 2014;22(3):138–146.
3. Guzman MG, et al. Dengue. Lancet. 2015;385(9966):453–465.
4. Comprehensive guidelines for prevention and control of dengue and dengue hemorrhagic fever. WHO SEARO 2011
Lecture 4
HOST RESPONSE TO INFECTION
Abstract
Infectious diseases are one of the leading causes of death worldwide. Many infectious diseases become difficult to control if the infectious agents evolve resistance to commonly used drugs, for example, bacteria can accumulate mutations in their DNA or acquire new genes that allow them to survive contact with antibiotic drugs that would normally kill them. Scientists are currently searching for new approaches to treat infectious diseases, focusing on exactly how the pathogens change and drug resistance evolves. Understanding and comprehend the host response to infection is important.
Infection process
After invading the body, microorganisms must multiply to cause infection. After multiplication begins, one of three things can happen:
1. Microorganisms continue to multiply and overwhelm the body’s defenses. 2. A state of balance is achieved, causing chronic infection.
3. The body—with or without medical treatment—destroys and eliminates the invading microorganism.
Defenses Against Infection
Host defenses that protect against infection :
– Natural barriers (eg, skin, mucous membranes)
– Nonspecific immune responses (eg, phagocytic cells [neutrophils, macrophages] and their products)
– Specific immune responses (eg, antibodies, lymphocytes)
Nonspecific Immune Responses
• Cytokines (including IL-1, IL-6, tumor necrosis factor-alpha, and interferon-gamma) are produced principally by macrophages and activated lymphocytes and mediate an acute-phase response that develops regardless of the inciting microorganism.
• The response involves fever and increased production of neutrophils by the bone marrow. Endothelial cells also produce large amounts of IL-8, which attracts neutrophils.
• The inflammatory response directs immune system components to injury or infection sites and is manifested by increased blood supply and vascular permeability, which allows chemotactic peptides, neutrophils, and mononuclear cells to leave the intravascular compartment.
Specific Immune Responses
• After infection, the host can produce a variety of antibodies (complex glycoproteins known as immunoglobulins) that bind to specific microbial antigenic targets. Antibodies can help eradicate the infecting organism by attracting the host’s WBCs and activating the complement system.
• The complement system destroys cell walls of infecting organisms, usually through the classical pathway. Complement can also be activated on the surface of some microorganisms via the alternative pathway.
Interaction between host and the microbes are depend on factors from the host, the microbes and environment
Host Genetic Factors
• For many pathogens, the host's genetic make-up influences the host's susceptibility and the resulting morbidity and mortality. For example, patients who have deficiencies of the terminal complement components (C5 through C8, perhaps C9) have an increased susceptibility to infections caused by neisserial species.
Factors Facilitating Microbial Invasion
Microbial invasion can be facilitated by the following:
• Virulence factors
• Microbial adherence, biofilm • Resistance to antimicrobials
• Defects in host defense mechanisms
Defects in Host Defense Mechanisms
Two types of immune deficiency states affect the host’s ability to fight infection: • Primary immune deficiency : are genetic in origin; > 100 primary immune
deficiency states have been described. Most primary immune deficiencies are recognized during infancy; however, up to 40% are recognized during adolescence or adulthood.
• Secondary (acquired) immune deficiency : are caused by another disease (eg, cancer, HIV infection, chronic disease) or by exposure to a chemical or drug that is toxic to the immune system.
Defects in immune responses may involve • Cellular immunity
• Humoral immunity
• Phagocytic system
• Complement system
Mechanism
• Cellular deficiencies are typically T-cell or combined immune defects. T
cells contribute to the killing of intracellular organisms; thus, patients with T-cell defects can present with opportunistic infections such as Pneumocystis jirovecii or cryptococcal infections. Chronicity of these infections can lead to failure to thrive, chronic diarrhea, and persistent oral candidiasis.
• Humoral deficiencies are typically caused by the failure of B cells to make
functioning immunoglobulins. Patients with this type of defect usually have infections involving encapsulated organisms (eg, H. influenzae, streptococci). Patients can present with poor growth, diarrhea, and recurrent sinopulmonary infections.
• A defect in the phagocytic system affects the immediate immune response
to bacterial infection and can result in development of recurrent abscesses or severe pneumonias.
• Primary complement system defects are particularly rare. Patients with this
type of defect may present with recurrent infections with pyogenic bacteria (eg, encapsulated bacteria, Neisseria sp) and have an increased risk of autoimmune disorders (eg, SLE).
• Most infections increase the pulse rate and body temperature, but others (eg, typhoid fever, tularemia, brucellosis, dengue) may not elevate the pulse rate commensurate with the degree of fever.
• Hypotension can result from hypovolemia, septic shock, or toxic shock. Hyperventilation and respiratory alkalosis are common.
• Alterations in sensorium (encephalopathy) may occur in severe infection regardless of whether CNS infection is present. Encephalopathy is most common and serious in the elderly and may cause anxiety, confusion, delirium, stupor, seizures, and coma.
• Infectious diseases commonly increase the numbers of mature and immature circulating neutrophils. Mechanisms include demargination and release of immature granulocytes from bone marrow, IL-1- and IL-6-mediated release of neutrophils from bone marrow, and colony-stimulating factors elaborated by macrophages, lymphocytes, and other tissues. Exaggeration of these phenomena (eg, in trauma, inflammation, and similar stresses) can result in release of excessive numbers of immature leukocytes into the circulation (leukemoid reaction), with leukocyte counts up to 25 to 30 × 109/L.
• Conversely, some infections (eg, typhoid fever, brucellosis) commonly cause leukopenia. In overwhelming, severe infections, profound leukopenia is often a poor prognostic sign.
• Characteristic morphologic changes in the neutrophils of septic patients include Döhle bodies, toxic granulations, and vacuolization.
• Anemia can develop despite adequate tissue iron stores. If anemia is chronic, plasma iron and total iron-binding capacity may be decreased. Serious infection may cause thrombocytopenia and disseminated intravascular coagulation (DIC).
Learning Tasks:
A 40 years-old female admitted to hospital with decreased of consciousness. She suffering from high fever since a week ago, and she also did not eat and drink much as for her weaknesses. She had headache, sometimes vomits and feel abdominal discomfort.
1. What is the working diagnosis of the patient?
2. What kind of examination do you need to do for this patient?
3. Please explain if there is a possibility of a defective imune response in this patient?
Self Assessment:
1. Describe the host response to infection in this patient.
Lecture 5
INFECTION IN PEDIATRIC
1. DENGUE HEMORRHAGIC FEVER References :
TatalaksanaDemam Dengue/DemamBerdarah Dengue Krugman’s Infectious Diseaseof Children
Nelson text book of Pediatrics
Abstract
Dengue hemorrhagic Fever (DHF) is a viral infection disease caused by dengue viral (DEN 1, DEN 2, Den 3 and DEN 4) with the symptom that are : fever 2 to 7 days, bleeding manifestation, enlargement of liver and shock with laboratory criteria thrombocytopenia and haemoconcentration. Four grade DHF from WHO are : grade I; fever with no specific symptom & Rumple Leed (RL) +, grade II; grade I + spontaneous bleeding, grade III; manifestation of circulatory failure and grade IV; profound shock.
Management DHF according of the grading of disease as well as suspicion DHF, DHF grade I, II and Dengue Shock Syndrome.
Learning Task
3 years old boys came with chief complaint high fever no decrease from three days ago, no cough and without sore throat. According to his parent he had vomited, no appetite no drink.
Task :
1. What are other helpful information you trying to get from his parent ? 2. What the physical examine you need to this patient ?
3. When the Rumple Leedepositive, what the kind of the laboratory test you have done ?
4. If the laboratory test showed leucopenic and trombositopenic, how about the management to this patient ?
Self Assessment:
1. What the clinical spectrum of dengue infection? Explain it ! 2. How about the patophysiology of Dengue Hemorrhagic Fever ? 3. Explain the pathogenesis of shock in DHF !
4. How the bleeding occur in DHF ?
5. Explain DHF clinicallyaccording the WHOcriteria ! 6. Explain the DHF complication !
7. How about the management of DHF? Explain it !
2. DIPHTHERIA References :
Krugman’s Infectious Diseaseof Chlidren Nelson text book of Pediatrics
Nelson Essentials of Pediatrics
Abstract
Diphtheria is a preventable acute disease caused by Corynebacterium Diphtheria. Diphtheria is acquired by contact with ill person with the disease or with an asymptomatic carrier of organism. The incidence increase among school age children during the first few month of the school year has been reported. Diphtheria usually develops after a short incubation period of 2 days with a range of 1 to 5 days. For clinical purposes, the disease my be classified by the anatomic location as a nasal diphtheria, tonsilar and pharyngeal diphtheria, laryngeal diphtheria, cutaneus diphtheria and unusual type of diphtheria. The diagnosis of diphtheria is confirmed by the demonstration of diphtheria bacilli cultured from material obtained from the site of infection. Diphtheria antitoxin must be given promptly and in adequate dosage. Penicillin and erythromycin are effective against most strains of diphtheria bacilli.
Supportive therapy is needed for several cases and complication. Preventive therapy by immunization with diphtheria toxoid.
Self Assessment
1. Explain the etiology of diphtheria ! 2. How the pathogenesis of diphtheria ?
3. Mention the sign and symptom that we could find in patient suffered from diphtheria based on the location of the infection !
4. Explain how to diagnosis diphtheria !
5. Mention the differential diagnosis of diphtheria based on the anatomic site of involvement !
6. Explain some severe complication caused by the effect of diphtheria toxin 7. Explain the management of diphtheria !
3. TETANUS
References :
Krugman’s Infectious Diseaseof Children Nelson text book of Pediatrics
Nelson Essentials of Pediatrics
Abstract
Tetanus is an acute, spastic paralytic illness caused by tetanus toxin; the neurotoxin produced by Clostridium Tetani. Tetanus occurs after induced spores germinate, multiply and produce tetanus toxin at infected injury site. Tetanus toxin binds at the neuromuscular junction and enter the motor nerve by endocytosis.
characterized by sudden, severe tonic contractions of the muscle. Diagnosis is established clinically with typical is an unimmunized patient who was injured or born within the preceding 2 week who presents with trismus, other rigid muscle and a clear sensorium. Management of tetanus requires eradication of C. tetani and the wound environment conductive to its anaerobic multiplication, neutralization of tetanus toxin, control of seizures and respiration, palliation and provision of meticulous supportive care. Penicillin G remains the antibiotic of choice for C. tetani, erythromycin and tetracycline (for patient 8 yr old or older) are alternatives for penicillin allergic patients. Muscle relaxants for relaxation and seizure control. Active immunization for prevent is tetanus toxoid usually combine with diphtheria and pertusis vaccine.
Self assessment
1. How is the characteristic of Clostridium tetani ? 2. Explain about portd’entrée of the bacteria !
3. How is the pathogenesis of stiffness caused by the effect of toxin in Tetanus ?
4. Mention the degree of tetanus and explain it ! 5. Mention the differential diagnosis of Tetanus ! 6. How is the management of patient with Tetanus ? 7. Explain some ways to prevent Tetanus!
4. MEASLES References :
Krugman’s Infectious Diseaseof Children Nelson text book of Pediatrics
Nelson Essentials of Pediatrics
Abstract
Measles is an acute, highly contagious viral disease characterized by fever, coryza, conjunctivitis, cough and a specific enanthem followed by a generalized
maculopapular eruption, caused by Morbillivirus, family Paramyxoviridae. After an incubation period (10 to 11 days) initial symptom is fever and malaise; within 24 hours there is onset of coryza, conjunctivitis and cough. The symptoms gradually increase in severity with the appearance of eruption on fourth day and koplik’s spot on 2 days before rash. Anorexia and malaise are usually present during the febrile period.
Measles is a self limiting disease therefore management is supportive therapy. The preventive with measles vaccination.
Self assessment
1. How the pathologic lesions process when the measles infection occurs ?
2. Explain the schematic diagram of clinical course of typical case of measles!
3. What is the etiology of measles?
4. How is the pathogenesis of measles?
6. Explain the management of patient with measles!
7. Explain how to prevent child from measles!
5. EMERGING DISEASE :AVIAN INFLUENZA References :
Avian Influenza WHO guideline
Abstract
Avian influenza (AI) is an infectious disease of birds by type A strain of the influenza virus. Mutation and reassortment (antigenic drift, antigenic shift) event are commonly observed in the affected birds populations. Since 2003, the widespread ongoing epizootic of AI A (H5N1) among poultry and birds has resulted in human H5N1 cases in 10 countries. The first cases of H5N1 virus infection in Indonesia was identified in July 2005. The reported symptoms of AI in humans have range from typical influenza like symptoms (eq, fever, cough, sore throat, and muscle aches) to eye infections (conjunctivitis), pneumonia, and other severe and live threatening complication. Patient was diagnosed confirmed case when we found positive viral culture for influenza A (H5N1) or positive for influenza (H5) or a four fold rise in H5 specific. Two drugs oseltamivir (Tamiflu® ) and zanamivir (Relanza® ) can reduce the severity and duration of illness.
Self Assessment
1. What is the etiology of Avian Influenza ?
2. What the clinical symptom human who infected avian viruses ? 3. How do people become infected ?
4. How can we safe to consumption the poultry product ? 5. Explain the pandemic hazard this virus !
6. Explain the management of patient with Avian Influenza ?
Lecture 6
TORCH INFECTION IN PREGNANT WOMEN
Abstract
Infections have historically been a major cause of maternal andfetal morbidity and mortality worldwide, and they remain soin the 21st century. The unique maternal-fetal vascular connectionin some cases serves to protect the fetus from infectiousagents, whereas in other instances it provides a conduitfor their transmission to the fetus.TORCH infectionsinclude infections associated with
Toxoplasma, Other organisms (Parvovirus, human immunodeficiencyvirus, Epstein-Barr virus, herpesviruses 6 and 8, varicella, syphilis, enteroviruses),
Rubella,Cytomegalovirus (CMV), and Hepatitis. Despite the recent emphasis in the screening, antibioticprophylaxis, and management of early-onset many neonates and children yearly experience the consequences of classic perinatal infections
Introduction
maternal-fetal vascular connection in some cases serves to protect the fetus from infectious agents, whereas in other instances it provides a conduit for their transmission to the fetus.Maternal serological status,gestational age at the time infection is acquired, the mode ofacquisition, and the immunological status of both the motherand her fetus all influence disease outcome.
TORCH is an acronym for a groupof congenitally acquired infectionsthat may cause significant morbidityand mortality in neonates. TORCH infections include infections associated with Toxoplasma, Other organisms (Parvovirus, human immunodeficiency virus, Epstein-Barr virus, herpesviruses 6 and 8, varicella, syphilis, enteroviruses), Rubella, Cytomegalovirus (CMV), and Hepatitis. Despite the recent emphasis in the screening, antibiotic prophylaxis, and management of early-onset many neonates and children yearly experience the consequences of classic perinatal infections.
Toxoplasmosis
The obligate intracellular parasite Toxoplasma gondii has a lifecycle with two distinct stages. The feline stage takesplace in the cat—the definitive host—and its prey. Unsporulatedoocysts are secreted in feces. In the non-feline stage, tissue cystscontaining bradyzoites or oocysts are ingested by the intermediatehost, including humans.Human infection is acquired by eating raw or undercookedmeat infected with tissue cysts or by contact with oocysts fromcat feces in contaminated litter, soil, or water. Prior infection isconfirmed by serological testing, and its prevalence depends ongeographic locale and parasite genotype.
Most acute maternal infections are subclinical and are detected only by prenatal or newbornserological screening. In some cases, maternal symptoms mayinclude fatigue, fever, headache, muscle pain, and sometimes amaculopapular rash and posterior cervical lymphadenopathy.The incidence and severity of fetal toxoplasmosis infectiondepend on gestational age at the time of maternal infection. Risksfor fetal infection increase with pregnancy duration A metaanalysis estimated the risk to be 15 percent at 13 weeks,44 percent at 26 weeks, and 71 percent at 36 weeks. Conversely, the severity of fetal infectionis much greater in early pregnancy, and these fetuses are muchmore likely to have clinical findings of infection.
Pregnant women suspected of having toxoplasmosis shouldbe tested. The parasite is rarely detected in tissue or body fluids.Anti-toxoplasma IgG develops within 2 to 3 weeks after infection,peaks at 1 to 2 months, and usually persists for life— sometimesin high titers. Although IgM antibodies appear by 10 days afterinfection and usually become negative within 3 to 4 months,they may remain detectable for years. Thus, IgM antibodiesshould not be used alone to diagnose acute toxoplasmosis. IgAand IgE antibodies are also useful in diagnosing acute infection.Toxoplasma IgG avidity increaseswith time. Thus, if a high-avidity IgG result is found, infectionin the preceding 3 to 5 months is excluded. Multiple commercialavidity tests are now available that provide a 100-percent positivepredictivevalue of high avidity confirming latent infection.
congenital toxoplasmosis risks.Treatment has been associated with a reductionin rates of serious neurological sequelae and neonatal demise.
Parvovirus
Human parvovirus B19 causes erythema infectiosum, or fifthdisease. The B19 virus is a small, single-stranded DNA virusthat replicates in rapidly proliferating cells such as erythroblast precursors. This can lead to anemia, which isits primary fetal effect. Only individuals with the erythrocytegloboside membrane P antigen are susceptible. In women withsevere hemolytic anemia—for example, sickle-cell disease— parvovirus infection may cause an aplastic crisis.
slappedcheekappearance. The rash becomes lacelike and spreads tothe trunk and extremities.Adults often have milder rashesand develop symmetrical polyarthralgia that may persist severalweeks.
There is vertical transmission to the fetus in up to a third ofmaternal parvovirus infections Fetal infection has been associated with abortion,nonimmune hydrops, and stillbirth. In a review of 1089 cases of maternalB19 infection from nine studies, Crane (2002) reportedan overall fetal loss rate of 10 percent. It was 15 percent forinfections before 20 weeks but was only 2.3 percent after 20weeks.
Depending on gestational age, fetal transfusion for hydropsmay improve outcome in some cases. Mortality rates as high as 30percent have been reported in hydropic fetuses without transfusions.With transfusion, 94 percent of hydrops cases resolvewithin 6 to 12 weeks, and the overall mortality rate is < 10 percent.Most fetuses require only one transfusion because hemopoiesisresumes as infection resolves.
There is currently no approved vaccine for human parvovirusB19, and there is no evidence that antiviral treatment prevents maternal or fetal infection. Decisionsto avoid higher-risk work settings are complex and requireassessment of exposure risks. Pregnant women should becounseled that risks for infection approximate 5 percent forcasual, infrequent contact; 20 percent for intense, prolongedwork exposure such as for teachers; and 50 percent for close,frequent interaction such as in the home. Workers at day-carecenters and schools need not avoid infected children becauseinfectivity is greatest before clinical illness. Finally, infectedchildren do not require isolation.
Rubella—German Measles
Maternal rubella infection is usually a mild, febrile illnesswith a generalized maculopapular rash beginning on the faceand spreading to the trunk and extremities. Other symptomsmay include arthralgias or arthritis, head and neck lymphadenopathy,and conjunctivitis. The incubation period is 12to 23 days. Viremia usually precedes clinical signs by about aweek, and adults are infectious during viremia and through 5 to7 days of the rash. Up to half of maternal infections are subclinicaldespite viremia that may cause devastating fetal infection.
Rubella may be isolated from the urine, blood, nasopharynx,and cerebrospinal fluid for up to 2 weeks after rash onset. Thediagnosis is usually made, however, with serological analysis.Specific IgM antibody can be detected using enzyme-linkedimmunoassay from 4 to 5 days after onset of clinical disease,but it can persist for up to 6 weeks after appearance of therash.Importantly, rubella reinfection cangive rise to transient low levels of IgM. Serum IgG antibodytiters peak 1 to 2 weeks after rash onset. This rapid antibodyresponse may complicate serodiagnosis unless samples are initiallycollected within a few days after the onset of the rash.If, for example, the first specimen was obtained 10 days afterthe rash, detection of IgG antibodies would fail to differentiatebetween very recent disease and preexisting immunity torubella. IgG avidity testing is performed concomitant with theserological tests above. High-avidity IgG antibodies indicatean infection at least 2 months in the past.
Rubella is one of the most complete teratogens, and sequelaeof fetal infection are worst during organogenesis. Pregnant women with rubella infection anda rash during the first 12 weeks of gestation have a fetuswith congenital infection in up to 90 percent of cases
At 13 to 14 weeks’ gestation, thisincidence was 54 percent, and by the end of the second trimester,it was 25 percent. Defects are rare after 20 weeks.
Cytomegalovirus
This ubiquitous DNA herpes virus eventually infects mosthumans. Cytomegalovirus (CMV) is the most common perinatalinfection in the developed world. Specifically, someevidence of fetal infection is found in 0.2 to 2.5 percent ofall neonates. The virus is secreted into allbody fluids, and person-to-person contact with viral-ladensaliva, semen, urine, blood, and nasopharyngeal and cervicalsecretions can transmit infection. The fetus may becomeinfected by transplacental viremia, or the neonate is infectedat delivery or during breast feeding.
Primary maternal CMV infection is transmitted to the fetusin approximately 40 percent of cases and can cause severe morbidity. In contrast, recurrentmaternal infection infects the fetus in only 0.15 to 1 percentof cases. A review of nine studies of CMV vertical transmissionrates reported first-trimester transmission in 36 percent, second-trimester in 40 percent, and third-trimester in 65 percent. Naturally acquired immunity during pregnancyresults in a 70-percent risk reduction of congenital CMV infection in future pregnancies. However, asnoted earlier, maternal immunity does not prevent recurrences,and maternal antibodies do not prevent fetal infection. Also,some seropositive women can be reinfected with a differentviral strain that can cause fetal infection and symptomatic congenitaldisease.
Several fetal abnormalities associated with CMV infectionmay be seen with sonography, computed tomography, or magneticresonance imaging. In some cases, they are found at thetime of routine prenatal sonographic screening, but in othersthey are part of a specific evaluation in women with CMVinfection. Findings include microcephaly, ventriculomegaly,and cerebral calcifications; ascites, hepatomegaly, splenomegaly,and hyperechoic bowel; hydrops; and oligohydramnios.
The management of the immunocompetent pregnant womanwith primary or recurrent CMV is limited to symptomatictreatment. If recent primary CMV infection is confirmed,amnionic fluid analysis should be offered. Counseling regardingfetal outcome depends on the gestation age during whichprimary infection is documented. Even with the high infectionrate with primary infection in the first half of pregnancy, mostfetuses develop normally.
There is no CMV vaccine. Prevention of congenital infectionrelies on avoiding maternal primary infection, especially inearly pregnancy. Basic measures such as good hygiene and handwashing have been promoted, particularly for women with toddlersin day-care settings. Although there maybe sexual transmission from infected partners, there are no dataon the efficacy of preventive strategies.
Hepatitis B
Chronic hepatitis B virus (HBV) infection is estimated to affect >350 million people worldwide and represents a significant cause ofmorbidity and mortality related to cirrhosis and hepatocellular carcinoma. Mother-to-child transmission (MTCT) of HBV remainsan important source of incident cases of HBV. Current barriers to eradication of incident HBV infections via MTCT include underutilizationof immunoprophylaxis with hepatitis B vaccination and hepatitis B immune globulin in certain endemic regions aswell as failure of immunoprophylaxis.
IU/mL), in whom therisk is highest, but transmission can occur even at levels>200 000 IU/mL. Treatment decisions necessitate careful discussionof risks and benefits as emerging data suggest some possibleeffect on bone mineral concentration in tenofovir-exposedpregnant women, which must be balanced by a nearly 10% riskof chronic infection with an incurable virus. Pregnant womenwith HBV must be monitored for clinical flares, with or withoutmedications, and breastfeeding should be allowed as well.
In the absence of HBV immunoprophylaxis, 10 to 20 percentof women positive for HBsAg transmit viral infection totheir infant. This rate increases to almost 90 percent if themother is HBsAg and HBeAg positive. Immunoprophylaxisand hepatitis B vaccine given to infants born to HBV-infectedmothers has decreased transmission dramatically and preventedapproximately 90 percent of infections.
Hepatitis C
Hepatitis C virus (HCV) is a well known cause of chronic liver disease in adults, but the burden of HCV inpregnant women and children is underappreciated. The leading route of HCV acquisition in children is verticaltransmission.
Women with chronic HCV infection often have uneventfulpregnancies without worsening of liver disease or othermaternal or infant adverse effects; some women mayeven have improvement. For example, in a series of 266pregnant women infected with HCV, elevated serum alanineaminotransferase (ALT) levels were detected in 56%of women at the beginning of pregnancy but only 7% during the third trimester. However, 55% of womenreturned to elevated ALT levels by 6 months postpartum.Such changes may be dueto the significant changes in the maternal immune systemduring pregnancy.
Infants born to women infectedwith HCV were more likely to be low birth weight, smallfor gestational age, and require neonatal intensive care andassisted ventilation. In the same cohort, women infectedwith HCV had an increased risk for gestational diabetesbut only when combined with excessive gestational weightgain.
There is currently no licensed vaccine for HCV prevention.The chronic HCV infection treatment has traditionallyincluded alpha interferon (standard and pegylated), aloneor in combination with ribavirin. This regimen is contraindicatedin pregnancy because of the teratogenic potential ofribavirin in animals.
Learning task
1. What is IgG avidity ? Who important this result for the treatment scenario ? 2. Describe about indication, side effect, effective dose, contra indication of
spiramycin ?
3. How to protect pregnant women from Parvovirus infection ? 4. Describe about MMR vaccination ?
5. How to protect pregnant women from Cytomegalovirusinfection ?
Self assement
1. Explain how to manage pregnant women with human immunodeficiency virus ?
3. Explain how to manage pregnant women with herpesviruses 6 and 8 ? 4. Explain how to manage pregnant women with varicella ?
5. Explain how to manage pregnant women with syphilis ? 6. Explain how to manage pregnant women with enteroviruses ?
Lecture 7
CENTRALNERVOUS SYSTEM INFECTIONS
MENINGITIS ANDENCEPHALITIS
AIMS:
Describe diagnosis, initial management and referral patients with meningitis and encephalitis
LEARNING OUTCOME:
1) Defineof meningitis and encephalitis
2) Describe prevalence of meningitis and encephalitis
3) Describe the most common signs and symptoms of meningitis and encephalitis 4) Describe the most common causes of meningitis and encephalitis
5) Describe common complication of Meningitis and Encephalitis 6) Explain the patophysiology of Meningitis and Encephalitis 7) Explain neurologic examination for meningitis and encephalitis 8) Discuss the need for urgent investigations and referrals
CURRICULUM CONTENS:
1. History taking patients with Meningitis and Encephalitis
2. Physical Examination patients with Meningitis and Encephalitis 3. Initial Management patients with Meningitis and Encephalitis
ABSTRACTS
Central nervous system (CNS) infections presenting to the em
