selected infectious diseases

1. DEPARTMENT OF PATHOLOGY AND FORENSIC
MEDICINE
FACULTY OF BASIC CLINICAL SCIENCE
COLLEGE OF HEALTH SCIENCE
UNIVERSITY OF ABUJA
EMERGING INFECTIOUS DISEASES
PRESENTED BY
16721001
16271129

2. OUTLINE
 INTRODUCTION
 DEFINITION
 EXAMPLES OF EMERGING INFECTIOUS
DISEASES
 FACTORS PREDISPOSING TO EMERGENCE
 BASIC CONCEPTS OF SELECTED EMERGING
INFECTIOUS DISEASES
 SUMMARY
 REFERENCES

3. INTRODUCTION
What are emerging infectious diseases?
 Emerging infectious diseases are diseases that have not
occured in humans before or that occured in small numbers in
isolated places.
 Or they are those whose incidence in humans has increased
in the past 2 decades or threaten to increase in the near
future.

4. Emerging and Re-emerging Infectious
Diseases
Emerging
 Have not occured in humans before.
 Have occurred previously but affected
some small numbers of people in
isolated places (AIDS and Ebola
hemorrhagic fever are examples)
 Have occurred throughout human history
but have only recently been recognized
as distinct diseases due to an infectious
agent and is rapidly increasing in
incidence or geographic range (Lyme
disease and gastric ulcers are
examples).
Re-emerging
 Diseases that once were major
health problems globally or in a
particular country, and then
declined dramatically.
 But are again becoming health
problems for a significant
proportion of the population

6. EXAMPLES OF EMERGING
INFECTIOUS DISEASES

7. YEAR RECOGNISED DISEASES INFECTIOUS AGENT
1937 WEST NILE INFECTION WEST NILE VIRUS
1967 MARBURG HEMORRHAGIC FEVER MARBURG VIRUS
1969 LASSA FEVER LASSA VIRUS
BEFORE 1976 SALMONELLOSIS SALMONELLA ENTERITIDIS
1977 CYCLOSPORA CYCLOSPORA CYATENESIS
1977 LEGIONNAIRE’S DISEASE LEGIONNAIRE PNEUMOPHILIA
1976 EBOLA HEMORRAGIC FEVER EBOLA VIRUS
1983 AIDS HUMAN IMMUNO-DEFICIENCY VIRUS
1983 GASTRIC ULCERS HELICOBACTER PYLORI
1989 HEPATITIS C HEPATITIS C VIRUS (HCV)
1998 NIPAH ENCEPHALITIS NIPAH VIRUS
2002 VRSA INFECTION VANCOMYCIN RESISTANT STAPHYLOCOCCUS
AUREUS
2003 SARS SARS CORONA VIRUS
2015 ZIKA VIRUS DISEASE ZIKA VIRUS
2019 COVID-19 SARS COV2 VIRUS

8. Factors Predisposing To Emergence
 Three major factors influence the emerging infectious diseases;
1-Environment;
 Ecological disruption and human intrusion into new ecological system,
usually tropical and developing countries are hotspots for outbreak of
diseases.
 Political conflict and breakdown of public health infrastructure.
2-Host
 Increased mobility and globalization.
 Decreased human immunity
3-Pathogen
 Evolution of the infectious agents such as mutations in bacterial genes that
confer antibacterial resistance e.g multidrug resistance TB and P.falciparum.

9. Basic concept of selected emerging
infectious diseases.
-Definition
-Epidemiology
-Predisposing factor
-Aetiopathogenesis
-Morphology
-Complication
-Prognosis

10. COVID-19
Definition
Corona virus was first identified as a cause of the common
cold in 1960. Until 2002, the virus was considered a
relatively simple, nonfatal virus.
• Coronavirus disease 2019 (COVID-19) is an
infectious disease mainly of respiratory system
caused by SARS-CoV-2.
• Started from “Wuhan City” of Hubei Province, China

11.  On January 30, 2020 WHO
declared the 2019–20
coronavirus outbreak to be a
Public Health Emergency of
International Concern
(PHEIC).
 COVID-19, named by WHO
on Feb 11, 2020 and the virus
was named as SARS corona
virus-2, belongs to the family
of coronavirus, the name to
crown-like spikes on their
surface.
 In march 2020 WHO declared
COVID 19 outbreak a
pandemic.

13. EPIDEMIOLOGY
By the end of October 2020, the severe acute respiratory syndrome
coronavirus 2 (SARS-CoV-2) pandemic had spread to 6 continents and
caused >45 million coronavirus disease (COVID-19) cases
and 1.1 million deaths.
Despite having 15.6% of the worldwide population, by October 31, 2020,
Africa had only 3.9% (1.76 million) of the world’s COVID-19 cases and
3.6% (42,233) of deaths during the pandemic.
Data suggest that the pandemic is evolving differently in sub-Saharan
Africa compared with the rest of the world and that the outbreak started
later.

14. Of note, severe COVID-19 cases seem to occur less frequently in
Africa than in the rest of the world. Several factors have been
proposed to explain this. Age is likely a major factor because older
persons are at higher risk for severe disease, but Africa has an
extremely young population; >60% of persons are <25 years of age.
However, variation of COVID-19 severity with age alone does not
fully explain the observed differences. Clinical cases and deaths in
Africa likely are underreported because systematic surveillance is
limited and no systematic death registration exists; thus, the true
SARS-CoV-2 burden probably is underestimated. Nevertheless,
local health systems in Africa, which have a lower capacity to deal
with COVID-19 patients than healthcare systems in high-resource
settings, were not overwhelmed, even at the peak of the epidemic.

15. PREDISPOSING FACTORS
 AGE
 Your chances of getting seriously sick with COVID-19 go up with your age. Someone
who’s in their 50s is at higher risk than someone in their 40s, and so on. The highest risk
is in people 85 and older.
 HEART PROBLEMS
 Heart failure, coronary artery disease, and heart disease raise your risk of severe illness.
 LONG-TERM KIDNEY DISEASE
 Dialysis can weaken your immune system so it doesn’t fight infections as well as it should.
 CANCER
 Your chances are higher if you currently have cancer. Experts aren’t sure whether the
same is true if you have a history of cancer.
 CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD)
 People with this long-term condition may already have lung damage that can make the
effects of COVID-19 worse.
 DIABETES, ASTHMA, OBESITY(BMI>30) AND SICKLE CELL DISEASE.

16.  AETIOLOGY
 Coronavirus tend to cause mild upper respiratory diseases in humans. Of the 7
known species of CoV, only 3 are known to cause severe infections in humans, all
within the betacoronavirus genus.
 An outbreak of severe acute respiratory syndrome coronavirus (SARS-CoV) in
2003 in Southern China from civet cats, caused an eventual 8,098 confirmed
cases, resulting in 774 deaths reported in 17 countries.
 In 2012, again another coronavirus Middle East respiratory syndrome coronavirus
(MERS-COV) from dromedary camels caused an outbreak in Saudi Arabia infected
2494 cases, resulting in 858 deaths with fatality rate 36%.
 SARS-COV-2: emerged in November 2019 in China from bats (still under
investigation). The genome is 96.2% identical to bat coronavirus RaTG13. It has
not yet been determined whether the virus is transmitted directly from bats or
through an unknown intermediate host.

17. VARIANTS OF COVID-19
 1. Alpha - Kent variant/B117
 Emerged in the UK in Kent in late September 2020.
 By the start of February 2021, it had soared to 96 per cent, causing a third
wave across the country.
 It also became dominant in the US.
 AstraZeneca-Oxford vaccine was 70.4 per cent effective against symptomatic
Covid-19 caused by the variant.
 Pfizer is 89.5 per cent effective against the strain, at least 14 days after the
second dose.

18.  2. Beta - South Africa variant/B1351
 This strain was first detected in South Africa in early October, but not publicly
announced until December 2020.
 It carries a mutation called E484K, which helps the virus elude a person’s
immune system.
 And the vaccines do not work as well against it
 In particular AstraZeneca, which offers only 10 per cent protection against mild
to moderate illness caused by the strain.

19.  3. Gamma - Brazil variant/P1
 This strain is believed to have emerged in mid-November (2020) in Brazil in the
Amazonian city of Manaus.
 Data collected in Manaus suggested the variant may be twice as transmissible
as previous strains, and could evade up to half of immune defences from
previous infections.

20.  4. Delta - Indian variant/B1617.2
 This was first detected in (2020) in India, where it led to a second wave that
has receded.
 The UK recently said it was estimated to be 40 per cent more transmissible
than the Alpha variant, which itself was also more transmissible than the
original strain.

21.  5. Epsilon - B.1.427/B.1.429
 It was first designated a variant of interest on March 5 and is common in
California.
 It is believed to be about 20 per cent more infectious.
 It carries the L452R mutation, which is believed to increase immune evasion
and binding to cells.

22.  6. Eta - B.1.525
 Eta was first detected in Nigeria but has since been found in other countries. It
was designated a variant of interest at the same time as Zeta.
 It includes the E484K mutation, which is believed to help the virus avoid the
immune system, and possibly vaccine-induced antibodies.

23.  7. Zeta - P2
 Identified as a a variant of interest later in March, it was discovered in Brazil in
April, 2020.
 It includes the E484 mutation in the spike.
 There is limited information on whether monoclonal antibody therapies and
antibodies generated post-vaccination are affected by it.

24.  8. Theta - P.3
 Theta was identified in the Philippines in January before being designated a
variant of interest in March. It also includes the E484K mutation.

25.  9. Iota - B.1.526
 The strain was detected in New York and identified as a variant of interest in
late March.
 There are two forms of the variant:
 E484K mutation
 S477N mutation
Believed to help the virus bind more tightly to cells.

26.  10. Kappa - B.1.617
 Detected in India in October, it was classified as a variant of interest in April. It
split into two lineages, one of which, B.1.617.2, has since become a variant of
concern.
 It carries two mutations believed to be of concern:
 L452R and E484Q
 termed as an escape mutation as it helps the virus slip past the body's
immune system.

27. Pathogenesis
The detail Pathogenesis of Covid-19 is
explained by the following steps:
A. Virus Entry and Spread
B. Acute Respiratory Distress Syndrome
(ARDS)
C. Cytokine Storm
D. Immune Dysfunction

28. A. VIRAL ENTRY AND SPREAD
 SARS-CoV-2 attaches to the host cell by binding its
Spike protein(S Protein) to the receptor protein,
angiotensin converting enzyme 2 (ACE2).
 ACE2 is expressed by epithelial cells of the intestine,
kidney, blood vessels, and, most abundantly, in type II
alveolar cells of the lungs.
 The human enzyme transmembrane protease, serine 2
(TMPRSS2), is also used by the virus for S protein
priming and to aid in membrane fusion.
 The virus then enters the host cell via endocytosis.

30. B. ACUTE RESPIRATORY
DISTRESS SYNDROME
 ARDS is a life-threatening
lung condition that prevents
enough oxygen from getting
to the lungs and into the
circulation, accounting for
mortality of most respiratory
disorders and acute lung
injury.

31.  More than 40 candidate genes including ACE2, interleukin
10 (IL-10), tumor necrosis factor (TNF), and vascular
endothelial growth factor (VEGF) among others have
been considered to be associated with the development
or outcome of ARDS.
 Increased levels of plasma IL-6 and IL-8 were also
demonstrated to be related to adverse outcomes of
ARDS.
 The above biomarkers suggest both a molecular
explanation for the severe ARDS and a possible treatment
for ARDS following SARS-CoV-2 infection.

32. c. CYTOKINE STORM
 The initial onset of rapid viral replication may cause
massive epithelial and endothelial cell death and
vascular leakage, triggering the production of
exuberant pro-inflammatory cytokines and
chemokines.
 Loss of pulmonary ACE2 function has been proposed
to be related to acute lung injury because ACE2
downregulation and shedding can lead to dysfunction
of the renin-angiotensin system (RAS), and further
enhance inflammation and cause vascular
permeability.

33.  A possible underlying mechanism of antibody-dependent
enhancement (ADE) has been proposed recently. ADE, a well-
known virology phenomenon, has been confirmed in multiple viral
infections.
 ADE can promote viral cellular uptake of infectious virus–antibody
complexes following their interaction with Fc receptors (FcR),
FcγR, or other receptors, resulting in enhanced infection of target
cells.
 The interaction of FcγR with the virus-anti-S proteinneutralizing
antibodies (anti-S-IgG) complex may facilitate both inflammatory
responses and persistent viral replication in the lungs of patients.

35. D. IMMUNE DYSFUNCTION
 Peripheral CD4 and CD8 T cells showed reduction and
hyperactivation in a severe patient.
 High concentrations of proinflammatory CD4 T cells and cytotoxic
granules CD8 T cells were also determined, suggesting antiviral
immune responses and overactivation of T cells.
 Additionally, several studies have reported that lymphopenia is a
common feature of COVID-19, suggestive of a critical factor
accounting for severity and mortality.

37. CLINICAL FEATURES

38. Morphology
GROSS
On examination, before the autopsy, only facial cyanosis was
noticed in both patients. Section of the thoracic cavity revealed
the lungs were contracted towards the hilus, cyanotic, and with
severely increased weight (case one: left lung 1000 grams,
right lung 1100 grams; case two: left lung 980 grams, right lung
1000 grams ). In both patients, the lungs fully sunk when
submerged underwater (positive lung float test). On cross-
section, the lungs were diffusely consolidated, without any
thrombi visible in the vasculature. The tracheas and bronchial
trees were edematous with severe erythema in the
interchondral areas of the mucosa.

40.  Pulmonary histopathology
 Histologically the lungs revealed evidence of acute respiratory distress syndrome (alveolar
hyaline membranes), interstitial (viral) pneumonia, and diffuse zones of hemorrhages
(Figures 1A, 1B). There was hyperplasia of type II pneumocytes, with the formation of
cytopathic syncytial cells and severe desquamation of bronchial respiratory epithelium as
well as two different sets of multinucleated cells (Figures 1C-1E).
 A: thick hyaline membranes (arrow), H&E stain, original magnification 400x; B: hemorrhagic
areas (arrows), H&E stain, original magnification 20x; C: type II pneumocyte hyperplasia
and syncytial cells (white arrows), and casts of desquamated respiratory epithelium (black
arrow) in the alveoli, H&E stain, original magnification 400x; D: viral cytopathic effect with
multinucleated cells (white arrow) and giant mononucleated cells (black arrows), H&E stain,
original magnification 400x; E: perivascular multinucleated cells (arrow), H&E stain, original
magnification 400x; F: endotheliitis - reactive endothelial cells (white arrows) and areas of
endothelial desquamation (black arrow), H&E stain, original magnification 400x; G: focal
fibroblast proliferation and alveolar space obliteration - organizing pneumonia (arrow), H&E
stain, original magnification 100x; H: degenerative and necrotic changes in peripheral
arterioles (arrows), H&E stain, original magnification 400.
 H&E: hematoxylin and eosin.

42. COMPLICATIONS

43. PROGNOSIS
Mortality: Several retrospective studies have reported variable
mortality from COVID-19-related acute respiratory distress
syndrome (ARDS).
Mortality appears lower than that in patients with severe acute
respiratory syndrome (SARS-CoV-1) or Middle East respiratory
syndrome (MERS).
The mortality from COVID-19 appears driven by the presence
of severe ARDS, and ranges widely, from 12% to 78% with an
average of 25% to 50%. However, death can occur from
several other conditions including cardiac arrythmia, cardiac
arrest, and pulmonary embolism.

44. TREATMENT

45. EBOLA
 DEFINITION
Also called Ebola Hemorrhagic Fever.
It is a severe, often fatal illness in humans. The virus is
transmitted to people from wild animals and spreads in the
human population through human-to-human transmission. The
average EVD case fatality rate is around 50%.
Ebola is a virus that causes problems with how your blood
clots. It is known as a hemorrhagic fever virus, because the
clotting problems lead to internal bleeding, as blood leaks from
small blood vessels in your body. The virus also causes
inflammation and tissue damage.

46. EPIDEMIOLOGY
 It is evident that since the first report of EVD, the number of ratified cases has increased
several folds. The causality cases of EVD almost doubled in Africa in comparison to the
earlier reported cases of the last four decades) and the cases reported between 2014 and
2016 (12,922 deaths out of 31,079 cases).
 The 2014–2015 outbreak was assumed to be the biggest epidemic in the history of this
disease. Though several strains of EBOV have been identified in the past, the 2014–2015
outbreak affecting mainly Western African countries (Guinea, Sierra Leone, Liberia, Senegal,
and Nigeria) was confirmed due to ZEBOV.
 Owing to its high virulence and fast transmission capability, it is categorized under ‘class A’
bio-weapon organism and thus making it essential to have real-time monitoring of EVD
cases and to look into any connectivity among the cases. For this, use of smart mobile
phones reporting of EVD cases in West Africa was encouraged by epidemiologists as an
effective technique. Use of social network analysis in this way will certainly help in
understanding disease spread in a better way.
 The case fatality rate observed in Ebola-affected cases in different countries varied between
25% and 100%.

49. PREDISPOSING FACTORS
 Travelling to Africa
 Animal research
 Health professionals treating infected patients
 Burial of dead body of infected person
 Handling of the following infected animals found ill/dead/
in the rain forest:
Chimpanzee, gorilla, fruit bats, monkeys, forest antelopes and
porcupines.

50. AETIOLOGY
 Ebola is caused by viruses in the Ebolavirus and Filoviridae family. Ebola is
considered a zoonosis, meaning that the virus is present in animals and is
transmitted to humans.
 How this transmission occurs at the onset of an outbreak in humans is
unknown.
 In Africa, people have developed Ebola after handling infected animals found
ill or dead, including chimpanzees, gorillas, fruit bats, monkeys, forest
antelope, and porcupines.
 Person-to-person transmission occurs after someone infected with
Ebolavirus becomes symptomatic. As it can take between 2 and 21 days for
symptoms to develop, a person with Ebola may have been in contact with
hundreds of people, which is why an outbreak can be hard to control and
may spread rapidly.

51. PATHOGENESIS
 Ebola virus enters the patient through mucous membranes, breaks in the skin, or
parenterally and infects many cell types, including monocytes, macrophages,
dendritic cells, endothelial cells, fibroblasts, hepatocytes, adrenal cortical cells, and
epithelial cells.
 The incubation period may be related to the infection route (6 days for injection
versus 10 days for contact). Ebola virus migrates from the initial infection site to
regional lymph nodes and subsequently to the liver, spleen, and adrenal gland.
Although not infected by Ebola virus, lymphocytes undergo apoptosis resulting in
decreased lymphocyte counts. ]
 Hepatocellular necrosis occurs and is associated with dysregulation of clotting
factors and subsequent coagulopathy. Adrenocortical necrosis also can be found
and is associated with hypotension and impaired steroid synthesis.

52. Ebola virus appears to trigger a release of pro-inflammatory cytokines with subsequent
vascular leak and impairment of clotting ultimately resulting in multiorgan failure and
shock.

53. CLINICAL FEATURES

54. MORPHOLOGY: GROSS
A–E, Representative gross pathology of Ebolavirus infection. All represented lesions were from Zaire ebolavirus–
infected ferrets; however, gross pathology severity was comparable across ebolavirus species. A, Pyloric
duodenal junction corresponding mucosal hemorrhage (arrow). B, Multifocal thymic hemorrhage (asterisk). C,
Multifocal hepatic necrosis. D, Splenomegaly, multifocal necrosis, and infarction (arrow).

55. MORPHOLOGY: MICROSCOPIC
(A) Hematoxylin and eosin stain showing intracytoplasmic eosinophilic
inclusions (arrow). (B) EM photomicrograph showing hepatic viral
inclusions (arrow).

56. COMPLICATIONS

57. PROGNOSIS
The prognosis of Ebola hemorrhagic fever is often
poor; the death rate of this disease ranges from 25%-
100%, and those who survive may experience the
complications listed above.
About half of the people who get Ebola die. The
survival rate has improved greatly since scientists
discovered Ebola in the 1970s. Previously, as many as
90% of sick people died. New antibody treatments offer
hope for survival rates to continue to improve.

58. TREATMENT
 Therapeutics
There are currently two treatments approved by the Food and
Drug Administration (FDA) to treat EVD. The first drug
approved in October 2020, Inmazeb™ external icon, is a
combination of three monoclonal antibodies. The second drug,
Ebanga™ external icon.
 Supportive Care
Providing fluids and electrolytes (body salts) orally or through
infusion into the vein
Using medication to support blood pressure, reduce vomiting
and diarrhea, and to manage fever and pain.

59. LASSA HAEMORRHAGIC
FEVER
 DEFINITION
 A viral hemorrhagic fever caused by the Arenavirus
Lassa, A single stranded RNA virus that is animal-
bourne. This was discovered following the death of
two nurses in Nigeria in 1969 and named after the
town in Borno state, Nigeria, where it was first
discovered.
 Transmitted from rodents to humans. The specis of
rats transmitting this disease is prevalent in West
Africa. (The multimammate rat’, mastomys
species_x0002_complex), and is pread via their urine
and droppings

60. There is secondary human to human transmission, via
body fluids exchange or in hospitals, via reused needles
or contaminated medical equipments. The virus can be
transmitted through direct contact with there materials
or via cuts and sores or via poorly stored food (as
Mastomys rodents are home scavengers). It can also be
airborne via inhalation of tiny particles in air
contaminated with rodents excreta.Also since mastomys
are consumed as food source, it may also occur via
direct contact when they’re caught and prepared for
food.

61. EPIDEMIOLOGY
 Its endemic in areas of West Africa including
Nigeria, Liberia, Sierra leone and Guinea.
 Annual incidence of 100,000 to 300,000 with
approximately 5,000 deaths in West Africa.
 Incubation period is 5-21days
 Its seasonal with clusters in late rainy and
early dry season.
 Affecting all age groups and sexes.

62. PREDISPOSING FACTORS
 The following are considered risk factors for
developing Lassa fever:
 Travel to endemic region (West Africa)
 Exposure to infected individuals
 Exposure to rodents (Mastomys natalensis
rat/mouse) or contaminated household items
(including food)
 Occupational exposure in healthcare settings

63. AETIOLOGY
 Once a Mastomys rat is infected with the virus, it can excrete the virus in its feces and
urine, potentially for the rest of its life.
 As a result, the virus can spread easily, especially as the rats breed rapidly and can
inhabit human homes.
 The most common method of transmission is by consuming or inhaling rat urine or
feces. It can also be spread through cuts and open sores.
 The rats live in and around human habitation, and they often come into contact with
foodstuffs. Sometimes people eat the rats, and the disease can be spread during their
preparation.
 Person-to-person contact is possible via blood, tissue, secretions or excretions, but not
through touch. Sharing needles may spread the virus, and there are some reports of
sexual transmission.
 Lassa fever can also be passed between patients and staff at poorly equipped hospitals
where sterilization and protective clothing is not standard.

64. PATHOGENESIS
 Endothelial cell damage/ capillary leak. Lassa virus
has an affinity for the vascular system, it first
presents as flushing, conjuctival injection, and
petechial haemorrhage associated with myalgias and
fever. Later frank mucous haemorrhage may occur.
 Platelet dysfunction
 Suppressed cardiac function

65. CLINICAL FEATURES

66. MORPHOLOGY: GROSS
 Axillary and inguinal lymphadenopathy and congestion. The mandibular and
mesenteric lymph nodes were also enlarged and noticeable enlargement and
congestion of the iliac lymph nodes was noted.
 Friable spleens and congestion at the ileocecal junction. Similar congestion and
enlargement of the inguinal, axillary, mandibular, and mesenteric lymph nodes
(Figure A) were also suggestive of LASV infection in all terminal animals.
 Congested or pale yellow, friable livers (Figure C); adrenal gland enlargement ;
pancreas enlargement; renal congestion ;
 Accumulation of red-tinged fluid in the pericardial sac(Figure B); congestion at the
ileocecal junction (Figure E);
 Petechial hemorrhage on the mucosal surface of the urinary bladder (Figure D).

68. MORPHOLOGY:MICROSCOPY
(A) Immunopositive endothelial cells (brown) in an axillary
lymph node

69. LASV immunostaining was noted in cells
morphologically consistent with dendritic cells primarily in
the marginal zone(of spleen)

70. lymphoplasmacytic and neutrophilic inflammation. LASV
antigen was detected in Kupffer cells and hepatocytes

71. PROGNOSIS
 The overall case-fatality rate is 1%. Among
patients who are hospitalized with severe
clinical presentation of Lassa fever, case-
fatality is estimated at around 15%. Early
supportive care with rehydration and
symptomatic treatment improves survival.

72. TREATMENT
 Drug of Choice: Ribavirin
 Most effective when started within first 6days of
illness.
 Its presently contraindicated in pregnancy but maybe
warranted if mother is at risk.
 Doesn’t reduce incidence of severity of deafness.
 Side effects are: reversible mild hemolysis,
headaches, and suppression of erythropioesis

73. ZIKA VIRUS DISEASE
 DEFINITION
 Zika virus is a mosquito-borne flavivirus discovered in Uganda
in 1947. The virus has emerged in recent years and spread in
the Pacific Area and the Americas.
 A disease caused by Zika virus that is spread through
mosquito bites.
 Zika virus disease (ZVD) has recently generated significant
concern globally.
 It was not considered a relevant human pathogen until the
large outbreak starting in Brazil in 2015 that revealed an
association of ZIKV infection with fetal microcephaly and
Guillain–Barré syndrome

74. DEFINITION CONT’D
 Zika virus (ZIKV) is a mosquito-borne flavivirus that
was first isolated in 1947 from the serum of a febrile
sentinel rhesus macaque (Macaca mulatta) in the Zika
Forest area located near Entebbe in Uganda, and
subsequently found also in Aedes africanus
mosquitoes in the same region

75. EPIDEMIOLOGY
 The very first known case of Zika fever was in a rhesus monkey in the
Zika Forest in Uganda in 1947.
 The first human cases were reported in Nigeria in 1954. A few outbreaks
have been reported in tropical Africa and in some areas in Southeast
Asia.
 The first major outbreak, with 185 confirmed cases, was reported in 2007
in the Yap Islands of the Federated States of Micronesia.
 In 2013 another large outbreak was reported in French Polynesia that
was thought to be from an independent introduction of the virus from Asia
than the Yap Island outbreak.
 In May 2015, the Pan American Health Organization (PAHO) issued an
alert regarding the first confirmed Zika virus infections in Brazil. Mosquito-
borne Zika virus is suspected to be the cause of 2,400 cases of
microcephaly and 29 infant deaths in Brazil in 2015.

77. PREDISPOSING FACTORS
 Living or traveling in countries where there have been
outbreaks. Being in tropical and subtropical areas increases
your risk of exposure to the Zika virus.
 Having unprotected sex. The Zika virus can spread from one
person to another through sex.

79. AETIOLOGY
 Zika virus disease is caused by a virus transmitted
primarily by Aedes mosquitoes, which bite during the
day.

80. PATHOGENESIS
 ZIKV replicates in the epithelial lining of midgut and salivary cells of the
mosquito vector. After a variable period of about 5 days, it appears in the
mosquito saliva which is now infectious. During blood meal, the vector
inoculates the virus into human host skin.
 The virus may then infect the epidermal keratinocytes, the fibroblast and
the Langerhans cells. Subsequently, viraemia ensues and the primary
target for of ZIKV is monocytes for both the Asian and African strains.

81. PATHOGENESIS CONT’D
 Monocytes have the potential to infiltrate immune sanctuary sites such as the brain,
testes and placenta.
 The immunological profile of ZIKV infection with the African lineage has a
classical/intermediate monocyte mediated M1-skewed inflammation, whereas the Asian
lineage has non-classical M2-mediated immunosuppression.
 Following viral transmission, viral attachment to the host cellular receptors is facilitated
by E glycoprotein.
 This is followed by endocytic uptake, uncoating of the nucleocapsid and viral RNA are
eventually released into the cytoplasm.
 In stark contrast to other flaviruses, its antigen has been demonstrated in host cell
nucleus.

82. CLINICAL FEATURES
 In about 80% of cases, ZIKV infection is asymptomatic. In patients with
symptoms, the disease presents as a febrile illness that may be
misdiagnosed as dengue or chikungunya.
 Among symptomatic patients, the most common symptoms include
macular or papular rash (90%), fever, typically low grade (70%), arthralgia
(60-70%), fatigue (70%), non-purulent conjunctivitis or conjunctival
hyperaemia (55%), myalgia (45%) and headache (45%), while other
symptoms, e.g. retro-orbital pain, oedema, vomiting, sore throat, uveitis
and lymphoadenopathy, are less frequent.

84. Guillain–Barré syndrome and other
neurological complications
 A case–control study on 42 GBS patients diagnosed between
November 2013 and February 2014 during the outbreak in
French Polynesia demonstrated that all GBS patients had
neutralising antibodies against ZIKV compared with 56% in the
control group of patients with febrile illness, and most had IgM
antibodies against ZIKV.
 This suggest that ZIKV was one of the causes of Guillain–
Barré syndrome.

85. ZIKV AND
PREGNANCY
Zika virus is a cause of
microcephaly and other severe
fetal brain defects.
• Defined by having a smaller
than normal head or brain
circumference
• Prognosis varies depending
on severity of microcephaly
• Brazil reporting increase in
number of babies with
microcephaly and some have
had lab-confirmed Zika
By preferentially destroying
radial glial cells, Zika virus can
produce severe microcephaly.

86. MORPHOLOGY
—a Segment of the agyric hemisphere shows an irregular surface with cobblestone appearance. b
meningeal glioneuronal heterotopia. The piamater is interrupted in some regions (arrows), with over-
migration of the cerebral tissue to the subarachnoid space (upper part of the picture). c —cerebral cortex
with polymicrogyria. d, e —very thin cerebral parenchyma

87. B--Medial view of one cerebral
hemisphere with thickened (arrow)
congested leptomeninges and
shallow sulci.
D--Medial surface of the cerebral
hemisphere with smooth surface and
collapsed occipital lobe due to
increased ventricle

88. PROGNOSIS
 The prognosis for most Zika virus infections
is good; however, complications such as
microcephaly, if proven to be related to the
infection in pregnancy, would be a poor
outcome for the newborn

89. TREATMENT
 There is no specific treatment for infection with the Zika virus.
 To help relieve symptoms, get plenty of rest and drink plenty of
fluids to prevent dehydration.
 Over-the-counter (OTC) medication acetaminophen (Tylenol,
others) may help relieve joint pain and fever.

90. SUMMARY
 Emerging infectious diseases are recently recognised or
recently occurring diseases.
 They have 3 major factors predisposing to their emergence;
environment, host and pathogen.
 Some major e.gs include COVID-19, Ebola HF, Lassa HF, and
ZIKA virus disease.

91. REFERENCE
 Amorosa V, MacNeil A, McConnell R, Patel A, Dillon KE, Hamilton K, et
al. Imported Lassa fever, Pennsylvania, USA, 2010. Emerg Infect Dis.
2010 Oct. 16 (10):1598- 600. [Medline]. [Full Text]. Chevalier MS, Chung
W, Smith J, Weil LM, Hughes SM.
 https://www.slideshare.net/ShaharulSohan/emerging-and-re-emerging-
infectious-diseases?qid=7dd7387f-8697-4047-89e7-
e9365d1b5b31&v=&b=&from_search=2
 Joyner SN, et al. Ebola virus disease cluster in the United States--Dallas
County, Texas, 2014. MMWR Morb Mortal.

92. REFERENCE CONT’D
 Wkly Rep. 2014 Nov 21. 63 (46):1087-8. [Medline]. Centers for Disease
Control and Prevention. Ebola (Ebola Virus Disease). CDC. Available at
https://www.cdc.gov/vhf/ebola/about.html. February 18, 2016; Accessed:
December 23, 2016. Sissoko D, Duraffour S, Kerber R, Kolie JS,
Beavogui AH, et al. Persistence and clearance of Ebola virus RNA from
seminal fluid of Ebola virus disease survivors: a longitudinal analysis and
modelling study. Lancet Glob
 Health. 2017 Jan. 5 (1):e80-e88.
 https://emedicine.medscape.com/article/830594-medication#showall

93. REFERENCE CONT’D
 Martinez-Pulgarin DF, Acevedo-Mendoza WF, Cardona-
Ospina JA, et al. A bibliometric analysis of global Zika
research. Travel Med Infect Dis 2016; 14:55–57.
 https://www.semanticscholar.org/paper/Zika-Virus-Associated-
with-Microcephaly.-Mlakar-
Korva/ee54ccf58c1137695a9d98b7357c1530969d024d
 https://www.thenationalnews.com/uae/health/what-are-the-
covid-19-variants-and-how-do-alpha-beta-and-delta-differ-
1.1236702

94. THANK YOU FOR
LISTENING