Module 4

Question 1

urban-wildlife interaction transmission

Answer 1

○ As human settlements expand into wildlife habitats, there is an increased risk of contact between humans and wildlife in urban areas

Question 2

cross-species transmission

Answer 2

○ Some pathogens undergo genetic changes, allowing them to adapt to new hosts
This can lead to cross-species transmission events

Question 3

leptospirosis

Answer 3

two species: Leptospira interrogans, which includes all pathogenic strains, and Leptospira biflexa, which contains non-pathogenic strains
The preferred reservoir host and incidental host vary with the strain as well as the geographic location.

Question 4

leptospira host range

Answer 4

Due to its extensive host range, affecting many wild and domestic animals, leptospirosis is one of the most prevalent zoonotic diseases globally. It is estimated that more than one million cases occur worldwide annually.

Question 5

Leptospira epidemiology

Answer 5

It is most common in tropical regions due to the pathogen’s ability to survive longer in warm, humid environments. Outbreaks often follow heavy rain and flooding.
The climate, population density, and the level of contact between maintenance hosts and incidental hosts, influences the spread of infection. A high population of maintenance hosts, inadequate sanitation and hygiene standards, as well as climate change linked to flooding are significant risk factors for infection in tropical nations. Additionally, many tropical nations have significant populations focused on agriculture, increasing the likelihood of human contact with infected animals

Question 6

Leptospira transmission

Answer 6

Animals can serve as either maintenance hosts or incidental hosts.
Humans are incidental hosts, as they only shed bacteria for a limited amount of time.
The disease is maintained through chronic infection of the renal tubules of maintenance hosts. Rats and mice are the most common, mostly asymptomatic, with the bacteria cleared from all organs except the kidneys. Humans can contract the infection through direct contact with the urine of infected animals or indirect contact with contaminated environmental samples
Human-to-human transmission is extremely rare.

Question 7

transmission of Leptospira for high risk groups

Answer 7

exposure at work or during leisure activities (sewer workers, farmers, swimmers, fishers, and athletes)
- direct contact: farmers, vets, etc. contact with infected animal
- indirect: sewer workers, miners, etc.

Question 8

Leptospira pathogenesis

Answer 8

Invasion:
○ Leptospira invades the body through non-intact skin, mucous membranes, or through ingestion of contaminated food and water. Once inside the body, it uses virulence factors to establish infection, including LPS, hemolysins, outer membrane proteins, other surface proteins, as well as adhesion molecules.
- Spread:
○ It is spread through the lymphatics and then into the bloodstream, homing to the liver and kidneys
- Persistence:
○ It can persist in some of the anatomically localized and immunologically privileged sites, like the renal tubule
○ Leptospires appear in the kidney 2-4 weeks after acute infection and attach to the brush border of the proximal renal tubular epithelium
- Excretion:
○ Animals may excrete leptospires intermittently or regularly for months, years, or a lifetime. humans do not remain carriers for long, but in cases where treatment is insufficient or nonexistent, leptospires can continue to shed in the urine for up to 3 months after infection

Question 9

clinical manifestation of Leptospira in animals

Answer 9

• Cats: infections are mostly asymptomatic
  
  • Cows, goats, and sheep: abortion, stillbirth, infertility, and haemolactia
  • Pigs: fever, abortion, stillbirth, jaundice, acute renal failure, and loss of appetite
  • Horses: fever, uvelitis, abortion, and acute renal failure
  • Marine Animals: increased drinking and urination, acute renal failure, vomiting, and reluctance to use their flippers
  • Dogs: fever, lethargy, vomiting, diarrhea, cough, jaundice, loss of appetite, and changes in urination frequency

Question 10

clinical manifestation of Leptospira in humans

Answer 10

The incubation period typically ranges from 7-12 days, but it can be as short as 3 days or as long as a month
- General Symptoms:
○ sudden onset of fever, chills, and headache, also muscle pain and tenderness.
- Eye Symptoms:
○ Conjunctival suffusion, marked by dilated conjunctival vessels without pus, as well as subconjunctival hemorrhages and jaundice.
- GI Symptoms:
○ Nausea, vomiting, diarrhea, and abdominal pain, which can worsen dehydration,

Question 11

severe Leptospirosis

Answer 11

dysfunction of organs such as the liver, kidneys, lungs, and brain, indicating an advanced infection stage. can manifest suddenly, affecting a significant portion of patients upon presentation.
Common symptoms of severe leptospirosis include jaundice and a widespread rash on the palms and the feet.

Question 12

Leptospira diagnosis

Answer 12

• Serology:
  the enzyme immunoassay uses an IgG and IgM ELISA kit, detecting antibodies against Leptospira spp. In serum
  Timing is important for this testing as antibodies for Leptospira develop between 3-10 days after symptom onset.
  
  • PCR:

Question 13

Leptospirosis treatment

Answer 13

The treatment depends on the severity of the disease.
The mild form of leptospirosis is rarely fatal, but the severe form (Weil’s disease) is associated with high mortality rates.
Early antibiotic treatment can decrease the severity and duration of the disease, therefore it is recommended to begin treatment in patients with a high clinical suspicion of leptospirosis without waiting for lab results.
Patients with severe leptospirosis usually need an intensive care unit admission as multiple organs can be affected and decompensation can occur rapidly.

Question 14

prevention and control of leptospira

Answer 14

source reduction (rodent control measures and animal vaccination)
environment and water sanitation
hygienic personal practices

Question 15

Y pestis

Answer 15

a non-motile, gram - bacilli bacterium.
Y pestis results in a severe, acute, and fast-progressing febrile illness with high mortality rates.
- causative agent of the plague

Question 16

forms of the plague

Answer 16

bubonic, septicemic, and pneumonic

Question 17

transmission of Y pestis to animals

Answer 17

through the bites of infected fleas, with rodents (rats) being the main hosts that maintain the bacterium in nature.
- other forms are direct contact and ingestion, but these are less common

Question 18

Y pestis flea born transmission

Answer 18

○ When an infected flea bites a host, it regurgitates the bacteria into the bite wound.
○ Environmental conditions can influence flea populations and their interaction with host species

Question 19

Y pestis direct contact and ingestion

Answer 19

○ less common
○ Carnivorous animals might contract the bacterium by eating infected rodents

Question 20

YP transmission in humans

Answer 20

Transmission can be from a variety of routes: flea bites (causing bubonic plague), respiratory droplets (causing pneumonic plague), contact with infected pets or domestic animals (causing conjunctivitis dermatitis, or pneumonia), and in rare cases, consumption of contaminated meat (causing gastroenteritis)

Handling sick or dead animals without PPE further increases the risk.

Question 21

YP pathogenesis

Answer 21

• Subcutaneous Infection:
  ○ Following the flea bit, the flea regurgitates the bacteria into the host’s skin while feeding
  
  • Migration to Lymph Nodes
    ○ The bacteria migrate to the nearest lymph nodes, where they begin to multiply rapidly
    ○ This often results in swollen and painful lymph nodes (buboes), characteristic of the bubonic plague
  • Lymphatic and Hematogenous Spread:
    ○ The bacteria can spread from the lymph nodes to the bloodstream (septicemia) and then to other organs, including the lungs (pneumonic plague)
  • Severe Inflammation:
    ○ The systemic infection triggers a strong inflammatory response, often leading to sepsis, disseminated intravascular coagulation, and multi-organ failure.

Question 22

clinical manifestations of YP in rodents

Answer 22

• Subacute:
  ○ Rodents affected by subacute plague may develop necrotic buboes and necrotic nodules in the liver, spleen, and lungs, succumbing to the disease six days or more after infection
  
  • Subacute and Acute:
    ○ nasal bleeding, small skin hemorrhages, abscess formation, and pneumonitis
    ○ The resolving form of the plague is characterized by lymph node enlargement, accompanied by localized pus filled necrosis
  • Acute:
    hemorrhagic buboes and splenomegaly, with death occurring within 3-5 days of infection, typically without other internal lesions present

Question 23

clinical manifestations of YP in humans

Answer 23

The incubation period of plague in humans lasts 2-6 days, marked by a sudden onset of fever, chills, headache, body ache, weakness, vomiting, and nausea.
Plague infections manifest in 3 forms based on the route of infection: bubonic, septicemic, and pneumonic.
- Bubonic:
○ Results from the bite of an infected flea
○ Characterized by swollen and painful lymph nodes (buboes), fever, chills, and headache
○ Without treatment, lethality rates range from 40-70% and can advance to pneumonic plague and fatal septicemia.
- Septicemic Plague:
○ Can occur if the bacteria is spread through the bloodstream, either from a flea bite or secondary to bubonic plague
○ widespread infection and inflammation, leading to fever, chills, abdominal pain, shock, and bleeding into the skin and other organs
○ Untreated, the fatality range is nearly 100%
- Pneumonic Plague:
○ Involves the lungs and presents with symptoms like cough, chest pain, difficulty breathing, and bloody/watery sputum
○ this form can be transmitted from person to person through respiratory droplets
○ Without early treatment, it has a near 100% mortality rate from respiratory failure and shock within 2 days

Question 24

YP diagnosis

Answer 24

cultures of clinical specimens and by serology that indicates a four fold rise in an antibody titer in patient serum

Question 25

YP treatment

Answer 25

Quick diagnosis and treatment are crucial Antibiotics and supportive care are effective against plague if administered promptly. First line antibiotics are Fluoroquinolones. Which antibiotic to use would be determined by susceptibility testing.

Question 26

YP prevention and control

Answer 26

vaccinations (only for high risk groups due to rarity of disease and treatability) isolate infected patients flea and rodent control (but killing of rodent vectors should be avoided to avoid fleas going to new hosts like humans) Surveillance in humans and animals

Question 27

managing plague outbreaks

Answer 27

To control the outbreak, prioritize starting vector control before rodent control, providing PPE to chemoprophylaxis to all health workers, and isolating pneumonic patients with masks to reduce airborne spread.

Question 28

Hantavirus

Answer 28

can lead to a range of clinical illnesses in humans around the globe typically associated with one or more rodent hosts There are many hantavirus strains with unique geographical distributions and clinical manifestations.

Question 29

hantavirus epidemiology

Answer 29

can be categorized into two groups: New World, which are endemic to the Americas, and Old World, primarily found in Europe and Asia.

Question 30

transmission of Hanta to animals

Answer 30

H establishes persistent infections in rodents, shrews, and bats, with each strain typically linked to a specific mammal reservoir, indicating a long term co-evolution. it can occasionally spill over to other rodents and bats. - Close Contact: ○ Transmission among rodents occurs through aerosols and close contact activities like biting, grooming, and sharing food, with the virus being shed in feces, saliva, and urine - Transplacental: ○ Uncommon, but infected rodents can harbour the virus for long periods, potentially for life - Indirect Conact: ○ Although dogs and cats do not carry hantaviruses, they can indirectly expose humans by bringing infected rodents into the home

Question 31

transmission of Hanta to humans

Answer 31

- Inhalation: ○ Humans can contract the virus by coming into contact with or inhaling particles from infected rodent urine, droppings, or saliva. Viral particles can become airborne when nesting materials are disturbed - Rodent Bite - Infected Surfaces: ○ Humans can contract the virus by touching surfaces contaminated with rodent urine, droppings, or saliva and then touching their nose or mouth - Contaminated Food: ○ Consuming food contaminated by an infected rodent's urine, droppings, or saliva can transmit the virus to a person

Question 32

hanta pathogenesis

Answer 32

Initial Infection: begins when h virus particles enter the body (usually inhalation). the virus first impacts alveolar macrophages in the lungs. virus then spreads through the bloodstream virus then goes to the lungs and kidneys, leading to endothelium infection Severe symptoms are caused due to host immune response leading to cytokine storm. cytokine storm causes increased vascular permeability, leading to leakage of lung and kidney fluids into tissues

Question 33

clinical manifestation of hanta

Answer 33

Antibodies against H have been reported in various animal species beyond rodents, (cattle, moose, cats, and dogs). However, reports of infections in animals in the wild are limited. In humans, New World H causes hantavirus pulmonary syndrome (HPS), while Old World H causes hemorrhagic fever with renal syndrome (HFRS), including its milder form, nephropathia epidemica (NE)

Question 34

HFRS

Answer 34

○ Incubation period of 7-36 days. About 10-15% of cases lead to severe symptoms, with mortality rates ranging from 6-15% ○ Clinical presentation varies from mild to severe, inducing systemic hemorrhagic manifestation ○ Renal involvement results in acute renal failure attributed to interstitial bleeding. The progression involves distinct clinical phases: febrile, hypotensive, oliguric, diuretic, and recovery ○ Manifestations encompass fever, lower back pain, abdominal discomfort, chills, muscle aches, fatigue, and slowed heart rate ○ Initially, patients may also experience conjunctival bleeding and vision disturbances

Question 35

HPS

Answer 35

○ The onset of HPS is marked by general flu symptoms (high fever, fatigue, muscle aches, and headaches) ○ Nearly hald of the HPS cases experience additional symptoms including dizziness, chills, and GI symptoms ○ After 4-10 days from the initial onset of illness, late symptoms fo HPS emerge, including coughing and shortness of breath due to acute pulmonary edema and hypotension ○ The mortality rate for HPS cases is about 50% ○ Patients who survive the acute phase typically recover within 5-7 days without any long term effects Acute renal failure can occur as a secondary complication due to shock and respiratory failure

Question 36

NE

Answer 36

○ In Europe, hantavirus Puumala is linked to NE, which has a mortality rate of 0.1% ○ NE manifests with sudden onset fever, headache, backache, abdominal pain, and hemorrhages ○ Renal involvement leads to transient proteinuria, haematuria, and renal dysfunction Acute renal failure occurs in many hospitalized patients, with a minority requiring transient hemodialysis.

Question 37

diagnosis of hanta

Answer 37

Diagnosing H infections in humans relies on: - Clinical Evidence/symptoms - Epidemiology Evidence: history of recent outdoor activity in endemic areas and rodent exposure - Laboratory Evidence: serology, RT-PCR, and immunochemistry

Question 38

treatment of hanta

Answer 38

There is no specific treatment of vaccine available for infection - Early detection of cases and proper medical care help in clinical improvement - The treatment regime is mostly supportive, and the patients can be intubated and given oxygen therapy to alleviate the phases of severe respiratory disease

Question 39

hanta prevention and control

Answer 39

- Prevention: ○ Avoiding close contact with rodents and contaminated areas - Control: ○ Controlling rodents by eliminating food sources, preventing entry to homes, and removing nesting sites ○ Wearing PPE when cleaning infested areas ○ Gloves and masks on while handling rodent traps or dead rodents

Question 40

influenza epidemiology

Answer 40

A: - Broad host range, inflecting various warm blooded animals (birds, pigs, horses, and humans), posing a significant risk of zoonotic transmission and potential epidemics B: - Primarily affects humans, but has been detected in seals C: - Mainly infects humans, occasionally pigs and dogs D: - Isolated from pigs originally, later found in cattle, its primary reservoir - Not known to infect or cause illness in humans

Question 41

avian influenza a epidemiology

Answer 41

These viruses are genetically diverse and widely distributed among wild avian species globally Wild waterfowl, primarily from ducks, geese, and swans serve as the natural reservoir AIA viruses can infect domestic poultry and other bird and animal species These viruses do not normally infect humans, but sporadic human infections have occurred - Cases of human infection from bird flu that infected a cow, humans exposed to the cow

Question 42

influenza cross species transmission

Answer 42

- Waterfowl to Poultry: ○ AIA in their natural reservoirs (waterfowl) are typically low pathogenic avian influenza, and mostly do not cause apparent symptoms ○ However, two of the 16 subtypes (H5 and H7) can evolve into highly pathogenic viruses, enabling interspecies transmission to domestic poultry and mammals - Birds to Humans: ○ H1N1, H2N2, and H3N2 have circulated in different geographical regions in humans ○ Recently, H5N1 and H7N9 have crossed the species barrier ○ None of these have escalated to epidemics, they demonstrate the potential for AIA to jump from birds to humans through transmission

Question 43

transmission of AI

Answer 43

3 primary routes: direct contact with infected birds, inhalation of droplets or dust in contaminated environments, or contact with contaminated surfaces - Transmission to Birds: AIA infects the respiratory and GI tracts and are shed in feces in birds. Wild birds, poultry, and mammals can become directly infected through exposure to the saliva, mucus, or feces of infected birds. They are primarily transmitted via fecal-oral route - Transmission to Humans: ○ Rare, because these viruses do not easily bind to receptors in the human upper respiratory tract ○ Howver, they can occur if sufficient amonuts of the virus enters a person's eyes, nose, or mouth, or is inhaled ○ This can happen when the virus is present in the air (droplets or dust), and a person breathes it in, or when a person touches a contaminated survace and then touches their eyes, nose, or mouth ○ AIA infections in people most often cocur after clsoe, prolonged, and unprotected contact without gloves or PPE with infected birds/animals

Question 44

pathogensis of AI

Answer 44

1. Attachment: The virus first attaches to host cells in the respiratory tract via its surface glycoprotein, HA. HA binds to sialic acid receptors on the surface of epithelial cells in the respiratory tract Once attached, the virus enters the host cell through receptor mediated endocytosis. 2. Transcription and Replication: Once inside the cell, the virion is transported to the nucleus, where viral RNA dependent RNA polymerase carries out the transcription and replication of viral RNA 3. Release: The new viruses assemble at the cell surface and are released when the NA glycoprotein cleaves sialic acid residues on host cell receptors, allowing newly formed virions to be released from the cell surface The released virions can infect neighbouring respiratory epithelial cells, continuing the cycle of infection and replication. The entire process from attachment to release typically takes about 6-8 hours. 4. Immune response: Viral replication triggers innate and adaptive immune responses, causing inflammation, tissue damage, and symptoms like fever, respiratory distress, and systemic effects

Question 45

clinical manifestation of AI in birds

Answer 45

Depending on host species, age, viral strain, and environmental conditions, susceptible birds may show a range of clinical manifestations. These symptoms can vary from sudden death without apparent clinical signs to more distinct symptoms - Neurological symptoms: uncoordination, nervous system symptoms - Skin and Physical Symptoms: bluish discolouration fo skin, wattls, and comb - Respiratory: ocular and nasal discharge, coughing, laboured breathing, and blood tinged discharge from nostrils - Behaviour and General Health: reduced vocalization, significant decease in feed and water consumption, diarrhea - Reproductive: decline in egg production

Question 46

classification of AIA in birds

Answer 46

Classifed by their molecular characteristics and ability to cause morbidity and mortality in lab chickens. There are 2 categories of viruses: Low Pathogenicity AI and High Pathogenicity AI - LPAI: subclinical to mild disease in chickens with a low mortality rate, few if any clinical signs in wild birds, and can mutate into highly pathogenic avian influenza - HPAI: severe disease and high mortality in chickens. Incubation period is 3-14 days. Moderate to severe clinical signs in wild birds. Few avian influenzas are HPAI, but H5 and H7 can cause 90-100% mortality in chickens. The virus can spill back into the wild leading to further spread during migration.

Question 47

clinical presentation of AI in humans

Answer 47

The incubation period in humans is shorter than in birds, with symptoms appearing about 2 days after the virus infects a person's respiratory tract. The symptoms of infection in humans include fever, malaise , cough, and muscle aches. Other early symptoms may include abdominal pain, chest pain, and diarrhea. The infection may progress to severe respiratory illness with symptoms including difficulty breathing or shortness of breath, pneumonia, acute respiratory distress syndrome, and neurological changes involving altered mental status or seizures. Whether the virus is classified as LPAI or HPAI does not predict human disease severity. Both can cause subclinical to severe disease depending on various factors.

Question 48

AI diagnosis in poultry

Answer 48

During poultry outbreaks, samples are collected through oropharyngeal and cloacal swabs (or feces) from live birds, along with feces and pooled organ samples from deceased birds. Virus detection methods can be employed such as agar gel immunodiffusion (AGID) and ELISA, as well as molecular tests like RT PCR. - Serological Tests: AGID and ELISA, used in poultry. Serve as surveillance purposes, and are not effective in diagnosing HPAI infections in highly susceptible birds, as these birds typically succumb to the virus before antibody development. Cross-reactivity between influenza viruses, such as in vaccinated versus unvaccinated birds, can also complicate serological test interpretation.

Question 49

AI diagnosis in humans

Answer 49

Samples used for the diagnosis of AIA virus in humans include respiratory tract samples or lung tissue, if obtained (biopsy, or post mortem) Influenza A and B are tested using RT-PCR.

Question 50

treatment of AIA

Answer 50

There is no specific treatment for influenza virus infections in animals and poultry. When poultry flocks are infected with HPAI, the standard procedure in HPAI-free countries involves depopulation. In contrast, various treatment options are available for humans. The treatment protocol for avian influenza in humans varies based on the severity of the case. Antiviral therapy is often combined with symptom management. The primary class of antiviral medications used to treat avian influenza includes neuraminidase inhibitors, such as oseltamivir

Question 51

prevention and control of AI in animals

Answer 51

outbreak management and vaccination: ○ Outbreak Management: § depopulation of infected flocks, combined with other measures such as movement, controls, quarantines, and emergency vaccination. § Insect and rodent control, disposal of contaminated material, and thorough cleaning and disinfection are also important to prevent the further spread of the virus ○ Vaccination: § Given the widespread distribution of certain strains, relying solely on culling for effective control is impractical § In many endemic areas, emergency vaccination programs or preventive measures are employed when the risk of a highly infectious strain is elevated.

Question 52

prevention and control of AI in humans

Answer 52

○ Prevention and control strategies include hygiene and PPE, as well as food safety and animal handling ○ Hygiene and PPE: § avoid contact wit sick animals and their environments. Practicing good hygiene is crucial. The use of appropriate PPE is strongly recommended § For individuals working with swine, maintaining proper hygiene and consistent use of PPE is equally important ○ Food Safety and Animal Handling: § In the case of an outbreak, it's critical to control the source of the virus (depopulation of infected birds, closing infected poultry markets, etc.) § Additionally, since HPAI viruses have been found in the meat and eggs of several avian species, careful food handling practices are important when working with raw poultry or wild game bird products in endemic areas. All poultry products, including wild birds, should be completely cooked before eating, as they may carry various viruses.

Question 53

ebola epidemiology

Answer 53

causes Ebola virus disease (EVD) in humans. - The average fatality rate of EVD is about 50%, but rates have varied from 25-90%. The absence of standard treatment and vaccination further exacerbates the threat posed by the Ebola virus.

Question 54

ebola zoonotic transmission

Answer 54

○ Humans can contract the Ebola virus through contact with tissues or fluids from infected animals ○ Droplet aerosol transmission has also been observed in animal models. Animal-to-human transmission may occur during hunting and consumption of reservoir species or infected non-human primates.

Question 55

human to human ebola transmission

Answer 55

○ Ebola outbreaks are sustained through secondary human-to-human transmission, primarily via exposure to blood, bodily excretions, and fluids like urine, feces, saliva, sweat, vomit, breast milk, semen, and vaginal fluids. Nosocomial transmission in healthcare settings is also a concern

Question 56

ebola sustained outbreak

Answer 56

○ The virus can persist in immunologically privileged sites within the body following acute infection, including the testes, the interior of the eyes, the placenta, and the CNS (specifically in CSF) ○ Even after recovery from acute infection, pregnant women may continue to carry the virus in breast milk or in pregnancy related fluids and tissues ○ Additionally, the virus can persist in the semen of individuals who have recovered from EVD, even if they did not experience severe symptoms.

Question 57

ebola pathogenesis

Answer 57

Results in immune suppression, causing lymphocyte apoptosis and weakening interferons, along with a systemic inflammatory response that cascades into multi-organ failure and shock - Initial Infection: ○ In the initial stages, the virus primarily replicates in monocytes, macrophages, and dendritic cells ○ These infected cells then migrate to regional lymph nodes, the liver, and the spleen, - Target Cells and Organs: ○ the inflammatory response leads to the activation of the endothelial cells that line the blood vessels, causing compromised vascular integrity, the release of tissue factor, and elevated nitric oxide levels (which can cause hypertension - Immune Response: ○ The activation of the endothelial cells lining the blood vessels leads to thrombocytopenia, often due to platelet loss from damaged tissues or virus induced disseminated intravascular coagulation, which further worsens the condition - Bleeding Complications: ○ This heightened immune response can lead to disseminated intravascular coagulation and acute hepatic dysfunction, both of which increase the risk of bleeding complications ○ Additionally, severe disease may result in acute kidney injury and pancreatitis, complicating the EVD management.

Question 58

clinical manifestation of ebola in animals

Answer 58

- Animals: ○ Incubation period of 2-14 days, followed by clinical signs like anorexia, coughing, bleeding, and death ○ In non-human primates, EVD has an extremely high mortality rate of nearly 100% ○ Fruit bats can be infected with the Ebola virus but remain asymptomatic, and as such, are considered the main reservoir species.

Question 59

clinical manifestation of ebola in humans

Answer 59

○ Longer incubation of up to 21 days, followed by fever, fatigue, muscle pain, headache, sore throat, vomiting, diarrhea, and signs of impaired kidney and liver function. These non-specific initial symptoms make early detection challenging As infection progresses, hemorrhagic signs, both internal and external, can be seen in 30-80% of patients. These may manifest as purpura, epistaxis, gingival bleeding, or GI bleeding.

Question 60

ebola diagnosis

Answer 60

Delayed diagnosis of EVD can escalate mortality rates, however the initial nonspecific symptoms of EVD present a clinical dilemma as they mirror symptoms of other infectious illnesses. Timely and accurate diagnostic testing in humans is crucial for controlling outbreaks. Beyond human samples, epidemiological surveillance initiatives may entail examining specimens from fruit bats and non-human primates to track its transmission and prevent spillover to human populations - Molecular Tests: gold standard is viral genome detection by RT PCR - Serological Tests: ELISA, detects host antibodies generated against the virus Clinical specimens obtained from patients, including blood, bodily fluids, and semen are considered biohazards.

Question 61

ebola treatment

Answer 61

Currently, there are no authorized antiviral medication specifically designated for treating individuals with EVD. Thus, the main strategy revolves around supportive care, encompassing hydration via oral or IV fluids, and symptomatic management Numerous potential treatments for EVD are currently undergoing assessment

Question 62

ebola prevention

Answer 62

Effective outbreak control strategies hinge on implementing a variety of interventions, such as case management, surveillance, contact tracing, robust laboratory services, safe burials, and organized social mobilization Community involvement is crucial for effectively managing EVD outbreaks, increasing awareness about the risk factors associated with Ebola infection and promoting preventive measures that individuals can implement is a potential method for curtailing human transmission

Question 63

ebola risk reduction

Answer 63

Mitigating wildlife-to-human transmission Mitigating human-to-human transmission (PPE): Outbreak Containment Measures (identification and monitoring): Mitigating possible sexual transmission/pregnancy: Vaccines: - Currently, two licensed vaccines are recommended for the prevention of Ebola in certain countries (ERVEBO and Zabdeno/Mvabea)