1 infectious diseases

INFECTIOUS DISEASES
BY
Dr.Tilahun Bizuayehu
UoG-Dept. of Internal M.
1

COURSE OUTLINE
1.Objectives
2.Introduction
3.Terminologies
4.Diagnostic techniques of infectious diseases
5.Protozoal causes of infectious disease
6.Helminths
7.Bacteria
8.Viruses
9.Fungus
2

1.OBJECTIVES
 General –at the end of the course the trainees should be able to;
 Know Public health significance of infectious diseases
 Understand the definition,epidemiology,life cycle,pathogenesis,clinical
manifestation,treatment and prevention of each specific disease entity
 Apply approaching techniques for the patient suspected of having
infectious disease/s
 Outline treatment plans
 Gain wisdom on infectious disease preventive strategies to his/her self
& to the patient in particular and to the general public in general
3

1.OBJECTIVES…
 Evaluation methods[applies for the whole course]
 Attendance -100%
 Class activity and medical ethics
 Quizs
 Oral exam
 Final written exam
References
1.Harrison’s principle of internal medicine 19th ed.
2.Davidson’s principle and practice of medicine 20th ed.
3.Medical microbiology, Jawetz 25th ed. 4

2.INTRODUCTION
 Q1.Origin of Infectious disease???[Louis Pasteur and Robert Koch]
 Q2.Germ theory of disease??? [Robert Koch]
 Infectious diseases remain the second leading cause of death
worldwide.
 These deaths disproportionately affect low- and middle income
countries
 In 2010, 23% of all deaths worldwide were related to infectious
diseases, with rates >60% in most sub-Saharan African countries.
 Given that infectious diseases are still a major cause of global
mortality, understanding the local epidemiology of disease is
critically important in evaluating patients.
 Diseases such as HIV/AIDS have decimated sub-Saharan Africa,
with HIV-infected adults representing 15–26% of the total
population.
5

2.INTRODUCTION…
 Moreover, drug-resistant tuberculosis is rampant
 The ready availability of this type of information allows physicians to
develop appropriate differential diagnoses and treatment plans for
individual patient
 Emerging and reemerging infectious diseases
 Globalization & infectious disease
 Global climate change &infectious disease
 Medical tourism
6

3.TERMINOLOGIES
 Infection
 Infestation
 Parasites
 Pathogen
 Vectors
 Hosts
 Associations b/n hosts & microorganisms
 Disease
 Nosocomial infection
 Life cycles
 Incubation period
 Normal flora 8

3.TERMINOLOGIES….
 Fever
 Dysentery vs diarrhea
 Sepsis
 Specimen vs sample
 Biologic signal
 Amplification
 wet mount
 Staining
 culture
9

4.DIAGNOSTIC TECHNIQUES OF INFECTIOUS DISEASES
approach to the patient
History
Physical Examination
Investigations
10

History
Exposure History
Exposure to drug resistance microbes
Social history
Dietary habits
Animal exposures
Travel history
Host-Specific Factors
immunity
medication 11

PHYSICAL EXAMINATION
Components???
G/A
Vital Signs
HEENT
Lipmhoglandular system
Respiratory
CVS
Gastrointestinal
Genitourinary
Integumentary
Musculoskeletal
CNS 12

Investigations
 Laboratory tests
 Blood
CBC
ESR
CRP
Blood film
Serologic tests
Culture 13

4.DIAGNOSTIC TECHNIQUES OF INFECTIOUS DISEASES…..
 Stool
-Gross
-Direct microscopy
-Concentration
Zinc sulphate[flotation]
Formole-ether- saline[sedimentstion]
Katokatz technique
-culture
14

 Urine
Gross
Chemical test
Microscopy
culture
15

 CSF
Gross
Chemical
Cytology
Microbilogic-wetmount,saining & culture
16

 Sputum
Gross
Acid fast stain for bacilus
Gram stain
gene expert………TB
culture??
17

 Other body fluids-eg,pleural,pericardial,ascetic,synovial fluids &body
discharges
Gross
Chemical
Cytology
Microbilogic-wetmount,saining & culture
18

 Skin
scraping-fungus[10% KOH]
snip-Onchocerciasis
Slit-Leprosy
19

5.PROTOZOAL INFECTIONS
5.1. Amebiasis and Infection with Free-Living Amebas
5.2. Giardiasis & Trichomoniasis
5.3. Malaria and HMS
5.4. Leishmaniasis
5.5. Toxoplasmosis
5.6. Trypanosomiasis
20

5.PROTOZOAL INFECTIONS…
5.1. Amebiasis and Infection with Free-Living Amebas
 5.1.1. AMEBIASIS
 Definition;
-an infection with the intestinal protozoan Entamoeba histolytica.
-about 90% of infections are asymptomatic, and the remaining 10%
produce a spectrum of clinical syndromes ranging from dysentery to
abscesses of the liver or other organs.
21

 LIFE CYCLE AND TRANSMISSION
-ingestion of viable cysts from fecally contaminated water, food, or
hands Motile trophozoites are released from cysts in the small
intestine[Excystation] After encystation, infectious cysts are
shed in the stool.
 EPIDEMIOLOGY
-About 10% of the world’s population is infected with Entamoeba, the
majority with noninvasive Entamoeba dispar.
E. histolytica is the third most common cause of death from parasitic
disease (after schistosomiasis and malaria).
22

Invasive colitis and liver abscesses are seven fold more common
among men than among women; this difference has been attributed to a
disparity in complement-mediated killing.
23

PATHOGENESIS AND PATHOLOGY
 only trophozoites of E. histolytica invade tissue
 Trophozoites attach to colonic mucus and epithelial cells by their lectin.
 This lectin is also thought to be responsible for resistance to complement-
mediated lysis.
 Once attached to the colonic mucosa, amebae release a cysteine-rich proteinase
that allows for penetration through the epithelial layer.
 Host cells are destroyed by 2 mechanisms: cytolysis and apoptosis.
 Cytolysis is mediated by trophozoite release of amoebapores (pore-forming
proteins), phospholipases, and hemolysins.
 Amoebapores may also be partially responsible for the induction of apoptosis, or
programmed cell death
 The earliest intestinal lesions are microulcerations of the mucosa of the cecum,
sigmoid colon, or rectum that release erythrocytes, inflammatory cells, and
epithelial cells
24

 Submucosal extension of ulcerations under viable-appearing surface
mucosa causes the classic “flask-shaped”ulcer containing
trophozoites at the margins of dead and viable tissues
 human intestinal infection is marked by a paucity of inflammatory
cells, probably in part because of the killing of neutrophils by
trophozoites. Treated ulcers characteristically heal with little or no
scarring.
 Occasionally, however, full-thickness necrosis and perforation occur.
 Rarely, intestinal infection results in the formation of a mass lesion or
ameboma.
25

Trophozoite of E. histolytica. A single
nucleus with a
central, dot-like nucleolus is seen
(trichrome stain]
Cyst of E.
histolytica. Three of
the four nuclei are
visible
(trichrome stain).
26

Appearance of ulcers on
colonoscopy 27

 Liver abscesses are always preceded by intestinal colonization,which
may be asymptomatic. Blood vessels may be compromised early by
wall lysis and thrombus formation. Trophozoites invade veins to reach
the liver through the portal venous system. E. histolytica is resistant to
complement-mediated lysis—a property critical to survival in the
bloodstream. In contrast, E. dispar is rapidly lysed by complement and
is thus restricted to the bowel lumen.
 The necrotic contents of a liver abscess are classically described as
“anchovy paste”
 Amebas, if seen, tend to be found near the capsule of the abscess.
 Amebic cysteine proteinases plays pivotal role in the pathogenesis.
28

 IgA plays a critical role in acquired immunity to E. histolytica but serum
IgG doesn’t.
29

 CLINICAL SYNDROMES
 Intestinal Amebiasis; The most common type of amebic infection is
asymptomatic cyst passage. Even in highly endemic areas, most
patients harbor E. dispar.
-Symptomatic amebic colitis develops 2–6 weeks after the ingestion of
infectious E. histolytica cysts. A gradual onset of lower abdominal pain
and mild diarrhea is followed by malaise, weight loss, and diffuse lower
abdominal or back pain.
30

-Cecal involvement may mimic acute appendicitis. Patients with full-
blown dysentery may pass 10–12 stools per day. The stools contain little
fecal material and consist mainly of blood and mucus. In contrast to
those with bacterial diarrhea, fewer than 40% of patients with amebic
dysentery are febrile. Virtually all patients have heme-positive stools.
More fulminant intestinal infection, with severe abdominal pain,
high fever, and profuse diarrhea, is rare and occurs predominantly in
children.
-Patients may develop toxic megacolon, in which there is severe bowel
dilation with intramural air.
- Patients receiving glucocorticoids are at risk for severe amebiasis.
31

 The association between severe amebiasis complications and
glucocorticoid therapy emphasizes the importance of excluding
amebiasis when inflammatory bowel disease is suspected.
 an asymptomatic or tender abdominal mass caused by an ameboma,
which is easily confused with cancer on barium studies. A positive
serologic test or biopsy can prevent unnecessary surgery in this
setting.
 Amebic Liver Abscess; Extraintestinal infection by E. histolytica most
often involves the liver.
32

-Most patients are febrile and have right-upperquadrant pain, which may
be dull or pleuritic in nature and may radiate to the shoulder. Point
tenderness over the liver and right-sided pleural effusion are common.
-Jaundice is rare.
-Although the initial site of infection is the colon, fewer than one-third of
patients with an amebic abscess have active diarrhea
-Since 10–15% of patients present only with fever,amebic liver abscess
must be considered in the differential diagnosis of fever of unknown
origin
33

 Complications of Amebic Liver Abscess Pleuropulmonary involvement,which
is reported in 20–30% of patients, is the most frequent complication of
amebic liver abscess.
 Manifestations include sterile effusions,contiguous spread from the liver,
and rupture into the pleural space.
 Sterile effusions and contiguous spread usually resolve with medical
therapy, but frank rupture into the pleural space requires drainage. A
hepatobronchial fistula may cause cough productive of large amounts of
necrotic material that may contain amebas. This dramatic complication
carries a good prognosis. Abscesses that rupture into the peritoneum may
present as an indolent leak or an acute abdomen and require both
percutaneous catheter drainage and medical therapy.
 Rupture into the pericardium, usually from abscesses of the left lobe of the
liver, carries the gravest prognosis; it can occur during medical therapy and
requires surgical drainage.
34

 Other Extraintestinal Sites
-The genitourinary tract may become involved by direct extension of
amebiasis from the colon or by hematogenous spread of the infection.
Painful genital ulcers, characterized by a punched-out appearance and
profuse discharge, may develop secondary to extension from either the
intestine or the liver. Both of these conditions respond well to medical
therapy. Cerebral involvement has been reported in fewer than 0.1% of
patients.Symptoms and prognosis depend on the size and location of
the lesion.
35

 DIAGNOSTIC TESTS
-Laboratory Diagnosis
- Stool examinations, serologic tests, and noninvasive imaging of the
liver are the most important procedures in the diagnosis of amebiasis.
-The definitive diagnosis of amebic colitis is made by the demonstration
of hematophagous trophozoites of E. histolytica.
-Culture & Biopsy???
Radiology,U/S,CT scan,MRI
36

 TREATMENT
- INTESTINAL DISEASE
Luminal agents- iodoquinol and paromomycin; Asymptomatic carriage
Systemic agents-metronidazole and tinidazole; Acute colitis
AMEBIC LIVER ABSCESS
-Metronidazole is the drug of choice for amebic liver abscess
 More than 90% of patients respond dramatically to metronidazole therapy
with decreases in both pain and fever within 72 h.
 Indications for aspiration of liver abscesses are;
(1) the need to rule out a pyogenic abscess, particularly in patients with
multiple lesions;
(2) the lack of a clinical response in 3–5 days;
(3) the threat of imminent rupture; and
(4) the need to prevent rupture of left-lobe abscesses into the pericardium. 37

 PREVENTION
Discussion???
38

 5.1.2.INFECTION WITH FREE-LIVING AMEBAS
 Free-living amebas of the genera Acanthamoeba and Naegleria are
distributed throughout the world
 ACANTHAMOEBA INFECTIONS-
 -Granulomatous Amebic Encephalitis follows a more indolent course and
typically occurs in chronically ill or debilitated patients,& Keratitis
 NAEGLERIA INFECTIONS-
 -Primary amebic meningoencephalitis caused by Naegleria fowleri follows
the aspiration of water contaminated with trophozoites or cysts or the
inhalation of contaminated dust, leading to invasion of the olfactory
neuroepithelium. Infection is most common among otherwise healthy
children or young adults, who often report recent swimming in lakes or
heated swimming pools
 TREATMENT
-treated with miltefosine 39

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