Clinical Microbiology: Flashcards
Important Bacterial and Viral causes of Community-Acquired Pneumonia by Age:
What are the risk factors of the typical organisms causing Community-Acquired Pneumonia?
Alcoholism is a risk factor of which pathogen to cause Community-Acquired Pneumonia:
Klebsiella Pneumonia and Oral Anaerobes
COPD is a risk factor of which pathogen to cause Community-Acquired Pneumonia:
Hemophilus Influenza
Which pathogen is associated with an increased risk of causing Community-Acquired Pneumonia in individuals with cystic fibrosis?
Pseudomonas aeruginosa
Which pathogen is associated with an increased risk of causing Community-Acquired Pneumonia in individuals with influenza virus infection or post influenza virus infection?
Staphylococcus Aureus
In individuals with history of bird exposure, particularly parrots, which pathogen poses a high risk of causing Community-Acquired Pneumonia?
Chlamydophila psittaci
Which virus is associated with Squamous cell laryngeal carcinoma and Squamous cell pharyngeal cancer:
🔸Human papillomavirus (HPV)
Low-risk subtypes: HPV 1, 2, 6 and 11
High-risk subtypes: HPV 16, 18, 31, and 33
JC Virus can cause:
🔸 Progressive Multifocal Leukoencephalopathy (PML)
The JC virus (JCV) is a type of human polyomavirus that was discovered in 1971. It is named after the initials of the patient, John Cunningham, from whom the virus was first isolated. The JC virus is a small, non-enveloped DNA virus that belongs to the Polyomaviridae family.
In the general population, the JC virus is quite common, with studies indicating that up to 70-90% of adults have been exposed to the virus at some point in their lives. After initial infection, the JC virus usually establishes a latent (inactive) infection in the kidneys and other sites, such as the bone marrow and lymphoid tissue.
In individuals with a healthy immune system, the JC virus typically remains dormant and does not cause any noticeable symptoms or complications. However, in people with weakened immune systems, such as those with HIV/AIDS, organ transplant recipients, or individuals with certain autoimmune conditions, the JC virus can become reactivated and cause significant health problems.
The most notable complication associated with JC virus reactivation is progressive multifocal leukoencephalopathy (PML).
- JC Virus Reactivation:
In individuals with HIV infection, the immune system is compromised, leading to a decreased ability to control viral infections. When the immune system is weakened, the JC virus can reactivate and start replicating in the brain. - Progressive Multifocal Leukoencephalopathy (PML):
PML is a rare but severe neurological condition caused by the JC virus. It primarily affects the white matter of the brain, leading to the destruction of myelin, the protective covering of nerve cells. As a result, individuals with PML can experience a range of neurological symptoms. - Clinical Presentation:
The symptoms of PML can vary depending on the areas of the brain affected. Common signs and symptoms may include:
- Changes in vision, such as blurred vision or loss of visual acuity.
- Difficulty with coordination, balance, and walking.
- Weakness or paralysis on one side of the body.
- Cognitive and behavioral changes, including confusion, memory loss, and personality changes.
- Speech problems.
- Seizures.
- Headache. - Diagnosis:
The diagnosis of PML involves a combination of clinical evaluation and diagnostic tests:
- Neurological Examination: A thorough neurological examination is performed to assess the individual’s symptoms and signs.
- Magnetic Resonance Imaging (MRI): An MRI scan of the brain is typically conducted to detect characteristic white matter lesions that are indicative of PML.
- JC Virus DNA Testing: Cerebrospinal fluid (CSF) samples may be collected and tested for the presence of JC virus DNA using a technique called polymerase chain reaction (PCR). - Management:
There is no specific antiviral treatment for PML, and the main focus is on managing the underlying HIV infection and supporting the individual’s immune system. This may involve the following:
- Antiretroviral Therapy (ART): Effective ART helps to restore the immune system function and control HIV replication, which can slow down the progression of PML.
- Immune Reconstitution Inflammatory Syndrome (IRIS): In some cases, as the immune system starts to recover with ART, an exaggerated inflammatory response can occur, which is known as IRIS. Treatment may involve medications to manage this immune response.
- Supportive Care: Symptomatic treatment is provided to manage specific symptoms and improve the individual’s quality of life. This may include physical therapy, speech therapy, and medications to control seizures or manage pain.
Explain Fifth Disease:
Fifth disease, also known as Erythema Infectiosum:
🔸Epidemiology:
Fifth disease is most commonly seen in children, particularly between the ages of 5 and 15 years. Outbreaks of the infection are more common during the winter and spring months. Adults can also be affected, especially those who are in close contact with infected children or have compromised immune systems.
Peak Incidence: 5 to 15 years old
🔸Transmission:
Parvovirus B19, the causative agent of Fifth disease, is primarily transmitted through respiratory droplets. It spreads from person to person through coughing, sneezing, or close contact with an infected individual. The virus can also be transmitted vertically from an infected mother to the fetus during pregnancy.
🔸Incubation Period:
The incubation period for Parvovirus B19 infection is typically 4-14 days, with an average of 10 days. This means that symptoms may appear within this timeframe after exposure to the virus.
🔸Clinical Presentation:
Fifth disease typically begins with a prodromal phase characterized by mild symptoms such as low-grade fever, headache, fatigue, and malaise. After a few days, the characteristic rash appears. It starts with a “slapped cheek” appearance, with bright red erythema on both cheeks, giving the face a flushed appearance. This is followed by a lacy, reticular rash on the trunk and extremities. The rash can be itchy but is usually not painful. The rash tends to fade over time, but it may reappear with heat, exercise, or sun exposure.
▪️Stage 1: Mild Symptoms
🔺Prodromal phase: characterized by mild symptoms such as low-grade fever, headache, fatigue, and malaise.
▪️Stage 2: Exanthem or Rash
It starts 2-5 days after the Mild or Prodromal Phase
The Rash first starts in the face with Slapped cheek rash and then extends to the trunk and extremities.
🔺Slapped-Cheek Rash: This rash involves the face with diffuse redness of the face with peri-oral sparing. 🔺Rash spread to Trunk and Extremities: Maculopapular rash, may be associated with pruritis in 50% of cases, fades after 7-10 days. Becomes more pronounced after exposure to sunlight or heat.
🔸Diagnosis:
All age groups may have transient normocytic anemia as Parvovirus B19 can affect the RBCs.
▪️Diagnosis in Immunocompetent Children:
🔺Clinical Diagnosis - Slapped Cheek rash
▪️Diagnosis in Immunocompetent Adults:
🔺If diagnosis is unclear we can do serology testing:
- IgM antibody
Appears within ∼ 10 days of initial exposure, indicating acute illness
Remains positive for 2–3 months - IgG antibody
Appears approx. 2 weeks following infection
Remains positive for life
▪️Diagnosis in Immunocompromised:
🔺Initial diagnostic test: viral DNA testing such as PCR of blood or bone marrow
🔺Adjunctive diagnostic test: serologic antibody testing
🔸Management:
In most cases, Fifth disease is a self-limiting condition that resolves on its own without specific treatment. Symptomatic management may include rest, hydration, and over-the-counter pain relievers to alleviate any discomfort.
Treatment is not necessary in most cases, as the disease is often self-limited
Analgesics and nonsteroidal anti‑inflammatory drugs (NSAIDs)
Short course of low‑dose prednisone for parvovirus B19‑associated arthritis
🔸Complications:
Fifth disease is generally a mild illness with a low risk of complications. However, certain populations, such as individuals with underlying immune deficiencies or pregnant women, may be at a higher risk of complications. In pregnant women, Parvovirus B19 infection can lead to fetal complications, including hydrops fetalis, as mentioned earlier.
Describe this picture, and what is the causative organism of this:
Slapped Cheek rash seen in Fifth disease
Caused by Parvovirus B19
Classification of Enveloped DNA Viruses:
Classification of Non-Enveloped DNA Viruses:
Explain Respiratory Syncytial Virus (RSV) and it’s course of Pathogenesis:
Respiratory Syncytial Virus (RSV) is a common viral infection that primarily affects the respiratory tract, particularly in young children. Let’s explore the details of RSV:
🔸Epidemiology:
RSV is a highly prevalent respiratory virus, and almost all individuals have had an RSV infection by the age of 2. Reinfection can occur throughout life due to the presence of different strains and waning immunity over time. This highlights the importance of continued preventive measures, especially in high-risk populations.
RSV infection can cause significant morbidity and mortality, particularly in young children and older adults. In young children, RSV is a leading cause of hospitalization, primarily due to bronchiolitis, which is the inflammation and obstruction of the small airways in the lungs. RSV bronchiolitis can lead to respiratory distress, difficulty breathing, and in severe cases, may require intensive care and mechanical ventilation. In older adults, RSV infection can also lead to severe respiratory illness, especially in those with underlying health conditions.
▪️RSV is the most common cause of hospitalization, bronchiolitis, and pneumonia in infants.
🔸Clinical Presentation:
- Symptoms of Nonspecific Viral Illness:
- Lethargy or fatigue: RSV infection can cause a general feeling of tiredness or lack of energy.
- Irritability: Infants and young children with RSV infection may become more irritable or fussy than usual.
- Decreased appetite: RSV infection can lead to a decreased desire to eat or drink.
- Fever: Fever is a common symptom of RSV infection, although not all individuals will experience it. The fever is usually mild to moderate in nature. - Symptoms of Upper Respiratory Tract Infection:
- Rhinorrhea: RSV infection can cause a runny nose, with the nasal discharge often being thick and copious in infants.
- Acute otitis media: Up to 60% of children with RSV infection may develop acute otitis media, which is an infection of the middle ear. This can present with symptoms such as ear pain, fever, and irritability. - Symptoms of Lower Respiratory Tract Infection:
- Cough: A persistent cough is a common symptom of RSV infection in patients of all ages.
- Tachypnea: RSV infection can lead to rapid breathing, known as tachypnea.
- Rales, wheezes, crackles: These abnormal lung sounds may be heard upon auscultation of the chest. Rales are crackling sounds, wheezes are high-pitched whistling sounds, and crackles are intermittent clicking or rattling sounds.
In Young Children:
- Clinical features of bronchiolitis: RSV infection commonly causes bronchiolitis in infants and young children. Bronchiolitis is characterized by inflammation and narrowing of the small airways in the lungs, resulting in wheezing, difficulty breathing, and respiratory distress.
- Clinical features of pediatric pneumonia: In some cases, RSV infection in young children can progress to pneumonia, which may present with symptoms such as fever, cough, rapid breathing, and signs of respiratory distress.
In Older Children and Adults:
- Clinical features of acute bronchitis: RSV infection in older children and adults may manifest as acute bronchitis, which is characterized by cough, production of sputum, and chest discomfort.
- Clinical features of pneumonia: RSV infection can also lead to pneumonia in older children and adults, with symptoms such as fever, cough, shortness of breath, and signs of pneumonia on clinical examination.
▪️Signs of Severe RSV Infection:
In severe cases of RSV infection, certain signs may indicate respiratory distress or severe illness:
- Signs of respiratory distress: These can include increased work of breathing, such as rapid or labored breathing, retractions (visible inward movement of the chest wall during inhalation), and nasal flaring.
- Hypoxemia: Severe RSV infection may lead to low oxygen levels in the blood, known as hypoxemia.
- Apnea: Episodes of temporary cessation of breathing, known as apnea.
🔸Transmission:
RSV is highly contagious and spreads through respiratory droplets when an infected person coughs or sneezes. It can also be transmitted through direct contact with surfaces contaminated by the virus. RSV is most prevalent during the fall, winter, and spring seasons.
▪️Incubation Period: 2-8 days
🔸Risk Factors:
▪️Risk factors for severe RSV infection in Children:
Age < 6 months: This is considered the single most important risk factor for severe RSV infection in children. Infants under 6 months of age have a higher risk of developing severe lower respiratory tract infection due to their immature immune systems and smaller airways.
Preterm birth, especially if associated with chronic lung disease of prematurity
Congenital heart disease
Immunocompromised states
Neuromuscular disorders that affect the ability to clear airway secretions
Childcare Attendance: Children who attend daycare or are in close contact with other children have a higher risk of RSV infection due to increased exposure to the virus.
Exposure to Tobacco Smoke: Secondhand smoke exposure can impair the respiratory defenses and increase the risk of severe RSV infection in children
▪️Risk factors for severe RSV infection in Adults:
Older age: ≥ 60 years (especially ≥ 75 years)
Chronic lung diseases: COPD, asthma
Cardiac diseases: congestive heart failure, coronary artery disease
Neurologic disorders: cerebrovascular disease, neuromuscular conditions
Diabetes mellitus
Chronic kidney disease
Liver disease
Hematologic disorders
Immunocompromised state
🔸RSV Virulence Factors:
▪️Fusion (F) Protein: The F protein is responsible for viral entry into host cells. It facilitates the fusion of viral and host cell membranes, allowing the virus to enter and infect respiratory epithelial cells. The F protein is a major target for neutralizing antibodies and plays a crucial role in RSV pathogenesis.
▪️Attachment (G) Protein: The G protein is involved in viral attachment to host cells. Although it is not essential for infection, it enhances viral infectivity and contributes to viral replication. The G protein also helps the virus evade the host immune response by interfering with the production of neutralizing antibodies. Glycoprotein G allows the virus to attach to respiratory epithelial cells; its ability to frequently mutate helps the virus evade the host immunity and permits reinfections throughout an individual’s life.
▪️RNA Polymerase: RSV encodes an RNA-dependent RNA polymerase that is crucial for viral replication and transcription of viral genes. This enzyme is essential for the production of viral RNA and proteins necessary for viral replication and assembly.
▪️Nonstructural Proteins: RSV produces nonstructural proteins, such as NS1 and NS2, which play a role in inhibiting the host immune response. These proteins interfere with the production of interferons, which are important antiviral molecules produced by the host cells to limit viral replication.
▪️Interferon Antagonism: RSV has developed mechanisms to counteract the host interferon response, which is a crucial defense mechanism against viral infections. The virus inhibits the production of interferons and interferon-stimulated genes, allowing it to replicate and spread within the host respiratory tract.
🔸Diagnosis:
Routine diagnostic testing for RSV is not usually done, but it can be considered depending on the clinical features. The decision to perform diagnostic testing may be considered by the presence of risk factors for severe RSV infection or the need for hospital admission and infection control measures.
- Additional Studies for Severe Illness: In cases of severe RSV infection, additional studies may be obtained to assess the severity of the illness. These studies can include arterial blood gas (ABG) analysis, respiratory viral panel, and chest x-ray. These tests help evaluate the respiratory status and assist in determining the appropriate management and treatment plan.
- Confirmatory Testing for RSV: If indicated based on clinical suspicion, confirmatory testing for RSV can be performed using various methods:
- Nucleic Acid Amplification Test (reverse transcription PCR): This is the preferred diagnostic method for RSV detection in respiratory tract samples.
- Rapid Antigen Detection Test: This test is primarily used in young children and provides quick results but may have slightly lower sensitivity compared to nucleic acid amplification tests.
- Viral Culture: Although rarely used due to its longer turnaround time, viral culture can also be used to identify RSV.
▪️Chest X-ray Findings: Chest X-ray is not routinely indicated in the diagnosis of RSV infection. However, in cases where a chest X-ray is obtained, it may show nonspecific findings such as peribronchial thickening and pulmonary hyperinflation. These findings are not specific to RSV infection but can be seen in bronchiolitis or pneumonia caused by RSV or other pathogens.
🔸Management:
Management of RSV infection focuses on supportive care to alleviate symptoms and prevent complications. This may include ensuring proper hydration, encouraging rest, using saline nasal drops to relieve nasal congestion, and providing fever-reducing medications if necessary. In severe cases, hospitalization may be required for close monitoring and respiratory support.
▪️Supportive Care:
Cool mist humidifier or steamy showers
Antipyretics for fever and/or discomfort
Encourage adequate fluid intake; if unable to tolerate oral fluids, provide NG/IV fluids.
Gentle nasal suctioning in infants
▪️Pharmacotherapy:
Infants and young children: inhaled ribavirin
🔸Prevention:
Preventing RSV infection is crucial, especially in high-risk individuals. Measures for prevention include frequent handwashing, avoiding close contact with sick individuals, covering the mouth and nose while coughing or sneezing, and disinfecting surfaces regularly. Additionally, for certain high-risk populations, a monthly injection of a monoclonal antibody called palivizumab may be recommended during RSV season for prophylaxis.
🔸Complications:
In infants and young children, RSV infection can lead to more severe respiratory symptoms, such as difficulty breathing, decreased appetite, and dehydration. It may also cause secondary bacterial infections, such as ear infections or pneumonia. In high-risk individuals, RSV infection can sometimes be life-threatening.
Respiratory Syncytial Virus (RSV) incubation period _______________.
2-8 days
What are the risk factors for developing Severe Respiratory Syncytial Virus (RSV) Infection in Adults and Children:
▪️Risk factors for severe RSV infection in Children:
- Age < 6 months: This is considered the single most important risk factor for severe RSV infection in children. Infants under 6 months of age have a higher risk of developing severe lower respiratory tract infection due to their immature immune systems and smaller airways.
- Preterm birth, especially if associated with chronic lung disease of prematurity
- Congenital heart disease
- Immunocompromised states
- Neuromuscular disorders that affect the ability to clear airway secretions
- Childcare Attendance: Children who attend daycare or are in close contact with other children have a higher risk of RSV infection due to increased exposure to the virus.
- Exposure to Tobacco Smoke: Secondhand smoke exposure can impair the respiratory defenses and increase the risk of severe RSV infection in children
▪️Risk factors for severe RSV infection in Adults:
- Older age: ≥ 60 years (especially ≥ 75 years)
- Chronic lung diseases: COPD, asthma
- Cardiac diseases: congestive heart failure, coronary artery disease
- Neurologic disorders: cerebrovascular disease, neuromuscular conditions
- Diabetes mellitus
- Chronic kidney disease
- Liver disease
- Hematologic disorders
- Immunocompromised state
What will Respiratory Syncytial Virus (RSV) infection show in Chest X-Ray:
Nonspecific findings such as peribronchial thickening and pulmonary hyperinflation
Respiratory syncytial virus can cause:
- Upper respiratory tract infections
- Bronchiolitis
- Pneumonia
Human metapneumovirus can cause:
- Bronchiolitis
- Pneumonia
Classification of Paramyxoviridae family which is under Enveloped RNA viruses:
Classification of Pneumoviridae family which belongs under Enveloped RNA Viruses:
When is the contagious period of Measles:
Measles is contagious for a period of 4 days before the onset of the characteristic rash (exanthem) and up to 4 days after the rash appears.
Peak incidence of measles:
Below 12 months of age
What is the Gold standard for the diagnosis of Measles:
Serology: Measles-specific IgM antibodies
What is the Pathogenesis of Measles:
🔸Epidemiology:
▪️Distribution: Measles tends to occur in regions with low vaccination rates and in resource-limited countries. This is because vaccination against measles has been highly effective in reducing its incidence in countries with widespread immunization programs. However, in areas where vaccination coverage is low or access to healthcare is limited, measles outbreaks can still occur.
▪️Peak Incidence: Measles is most commonly seen in children under 12 months of age. This is because infants in this age group are particularly susceptible to infection due to their immature immune systems and lack of protective antibodies. However, measles can affect individuals of all ages who are not immune to the virus.
▪️Infectivity: Measles is highly contagious, with an infectivity rate of approximately 90%. This means that if an individual with measles comes into contact with 10 susceptible individuals, around 9 of them are likely to become infected. The virus can be transmitted through respiratory droplets when an infected person coughs or sneezes. Importantly, measles is contagious for a period of 4 days before the onset of the characteristic rash (exanthem) and up to 4 days after the rash appears. This makes it possible for the virus to spread even before an individual realizes they are infected.
▪️Risk Factors: Certain individuals are at an increased risk of acquiring or transmitting measles, mumps, and/or rubella. These include:
- Individuals with an immunocompromised state: People with weakened immune systems, such as those with HIV/AIDS or undergoing immunosuppressive therapy, are at higher risk of severe complications if they contract measles. They are also more likely to transmit the virus to others.
- Household or close contacts of immunocompromised individuals: People living or in close contact with individuals who are immunocompromised are at increased risk of acquiring measles and transmitting it to others, especially if they are not immune or have not been vaccinated.
- College students: College campuses, with their close living quarters and frequent social interactions, can facilitate the spread of measles among susceptible individuals who may not have been previously vaccinated or exposed to the virus.
- Health care personnel: Healthcare workers who come into contact with infected individuals are at an increased risk of acquiring measles. This highlights the importance of maintaining up-to-date vaccinations among healthcare professionals to protect both themselves and their patients.
- International travelers: Measles can be imported into countries where the disease is no longer endemic through international travel. Unvaccinated individuals traveling to areas with ongoing measles outbreaks are at risk of acquiring the virus and potentially spreading it to others upon their return.
🔸Etiology
- Pathogen: measles virus (MV), an RNA virus of the Morbillivirus genus belonging to the Paramyxoviridae family
- Route of transmission: direct contact with or inhalation of virus-containing droplets
🔸Clinical Features:
♦️Stage 1 or Prodromal stage, also known as the Catarrhal stage:
Duration: The prodromal stage typically lasts for about 4-7 days [4]. This stage occurs before the onset of the characteristic rash associated with measles.
Presentation: During the prodromal stage, several symptoms and signs can be observed, including:
- Coryza: This refers to a runny or stuffy nose, often accompanied by nasal congestion and sneezing.
- Cough: A persistent cough is commonly seen during this stage.
- Conjunctivitis: Inflammation of the conjunctiva, the thin membrane covering the white part of the eye and inner surface of the eyelids, can cause redness, itching, and discharge.
- Fever: Measles is typically associated with a high fever during the prodromal stage.
Koplik Spots: One of the characteristic findings of measles during the prodromal stage is the presence of Koplik spots. These are pathognomonic enanthem. Koplik spots are tiny white or bluish-gray spots that appear on an irregular erythematous (red) background. They are most commonly found on the buccal mucosa, which is the inner lining of the cheeks. The spots resemble grains of sand and are often described as “salt sprinkled on a wet background”. Koplik spots typically disappear by the second day of the exanthem stage, which is when the rash appears.
The presence of Koplik spots is highly suggestive of measles and can aid in the early diagnosis of the disease. However, it’s important to note that not all individuals with measles will develop Koplik spots, and their absence does not rule out the diagnosis.
♦️Stage 2 or Exanthem Stage:
Duration: The exanthem stage of measles typically lasts for about 7 days and develops 1-2 days after the Koplik spots.
Presentation: During the exanthem stage, several symptoms and signs can be observed, including:
- High fever: Measles is associated with a high fever during the exanthem stage.
- Malaise
Generalized Lymphadenopathy: Measles can cause swelling and tenderness of the lymph nodes throughout the body. This is referred to as generalized lymphadenopathy.
Erythematous Maculopapular Exanthem: The characteristic rash of measles appears during the exanthem stage. It is described as erythematous, meaning it is red, and maculopapular, which means it consists of flat, reddened areas (macules) and raised, small bumps (papules). The rash is blanching, which means it temporarily fades when pressure is applied and then returns when the pressure is released.
Rash Progression: The rash typically starts behind the ears along the hairline and then spreads to the rest of the body, moving downward towards the feet. It is important to note that involvement of the palms and soles is rare in measles.
Rash Resolution: The rash gradually fades after about 5 days from its onset. As it fades, it may leave behind a brown discoloration and desquamation (peeling of the skin) in more severely affected areas.
The presence of the characteristic erythematous maculopapular rash, along with the other symptoms and signs described, is highly suggestive of measles. However, it is important to remember that the diagnosis of measles should be confirmed through appropriate diagnostic testing.
♦️Stage 3 or Recovery Stage:
The cough may persist for another week and may be the last remaining symptom.
🔸Diagnostics
Measles should be suspected in a patient with typical clinical findings, but Laboratory tests are always necessary to confirm the diagnosis.
- CBC: ↓ leukocytes, ↓ platelets
- Serology:
Gold standard: detection of Measles-specific IgM antibodies.
These IgM antibodies appear after the onset of Exanthem. False-Positives may occur with Parvovirus B19 and Rheumatoid Factor.
IgG antibodies
- Identification of pathogen: direct virus detection via reverse-transcriptase polymerase chain reaction (RT-PCR) possible
- Biopsy: affected lymph nodes show paracortical hyperplasia and Warthin-Finkeldey cells (multinucleated giant cells formed by lymphocytic fusion).
🔸Management:
- Symptomatic management
- Vitamin A supplementation: Reduces morbidity and mortality
- Isolate patients with confirmed infection.
- All patients: Isolate for 4 days from the onset of rash (longer if immunocompromised).
- Hospitalized patients: Initiate airborne precautions.
- Measles is a nationally notifiable disease; report all cases to the appropriate health departments within 24 hours.
🔸Complications:
Bacterial superinfection causing:
Otitis media
Pneumonia (most common cause of death)
Laryngotracheitis
Explain Mumps Pathogenesis:
🔸Epidemiology:
Peak age: 5–14 years of age
Sex: ♂ = ♀ for parotitis (however, males are three times more likely to have CNS complications)
🔸Etiology
Mumps is caused by the mumps virus, which belongs to the Paramyxoviridae family. The virus is a single-stranded RNA virus and is the pathogen responsible for mumps infection.
Transmission: Mumps is transmitted from person to person through various means, including:
- Airborne droplets: The virus is primarily transmitted through respiratory droplets when an infected person coughs, sneezes, or talks. These droplets contain the virus and can be inhaled by individuals in close proximity to the infected person.
- Direct contact with contaminated saliva or respiratory secretions: Mumps can also be transmitted through direct contact with infected saliva or respiratory secretions. This can occur through activities such as sharing utensils, kissing, or close personal contact.
Utensils: Utensils, in the context of mumps transmission, refer to objects used for eating or drinking, such as forks, spoons, glasses, or cups. If an individual with mumps uses a utensil and then another person uses the same utensil without proper cleaning, the virus can be transferred from the infected person’s saliva or respiratory secretions to the utensil. If the second person then uses the contaminated utensil and touches their mouth, nose, or eyes, they can become infected with the mumps virus. - Contaminated fomites: Fomites are inanimate objects that can become contaminated with the virus. If a person touches a contaminated surface, such as a doorknob or a tissue, and then touches their mouth, nose, or eyes, they can become infected with the mumps virus.
Contagious period: Affected individuals are contagious approximately 3 days before the onset of symptoms, which can include fever and malaise, and continue to be contagious for up to 9 days after the parotid gland becomes swollen.
🔸Pathophysiology:
1. Nasopharyngeal entry: The mumps virus enters the body through the nasopharynx, which is the upper part of the throat behind the nose. This can occur when an individual inhales respiratory droplets containing the virus, typically from an infected person who coughs or sneezes nearby. The virus establishes its initial infection in the mucous membranes of the nasopharynx.
- Replication in mucous membranes and lymph nodes: Once inside the body, the mumps virus begins to replicate within the mucous membranes of the nasopharynx. The virus attaches to specific receptors present on the surface of the host cells and enters them. Once inside the cells, the virus uses the host’s cellular machinery to produce viral proteins and genetic material, leading to the production of more viral particles.
Simultaneously, the virus also gains access to nearby lymph nodes. Lymph nodes are part of the body’s immune system and play a crucial role in filtering and monitoring the lymphatic fluid. The mumps virus is carried by immune cells called lymphocytes from the initial infection site to the lymph nodes. Within the lymph nodes, the virus continues to replicate, leading to the further production of viral particles.
- Viremia and secondary infection of salivary glands: Following replication in the mucous membranes and lymph nodes, the mumps virus enters the bloodstream, resulting in viremia. Viremia refers to the presence of the virus in the blood. Through the bloodstream, the virus can reach various organs and tissues throughout the body.
One of the primary targets of the mumps virus is the salivary glands, particularly the parotid glands. The parotid glands are the largest of the salivary glands and are located on the sides of the face, in front of the ears. The virus infects the glandular cells within the parotid gland, causing inflammation and swelling. This swelling of the parotid gland is characteristic of mumps and can be visibly observed as swelling around the jawline and cheeks.
- Further dissemination: While the primary site of infection is the parotid gland, the mumps virus can potentially spread to other organs and tissues in the body. This secondary dissemination occurs through the bloodstream and can involve various glands and organs.
- Lacrimal glands: The virus can infect the lacrimal glands, which are responsible for tear production. This can lead to inflammation and swelling of the lacrimal glands, resulting in dry eyes or eye redness in some individuals with mumps.
- Thyroid gland: The thyroid gland, located in the neck, can also be affected by the mumps virus. Infection of the thyroid gland can result in thyroid inflammation (thyroiditis) and may cause symptoms such as neck pain or discomfort.
- Mammary glands: In some cases, the mumps virus can disseminate to the mammary glands, which are responsible for milk production in females. This can lead to breast inflammation (mastitis) in affected individuals.
- Pancreas: The mumps virus can infect the pancreas, an organ located in the abdomen that plays a crucial role in producing insulin and regulating blood sugar levels. Pancreatic infection can cause pancreatitis, an inflammation of the pancreas, which may result in abdominal pain, nausea, and vomiting.
- Testes and Ovaries: Mumps can also affect the reproductive organs. In males, the virus may infect the testes, leading to orchitis (inflammation of the testicles). Orchitis can cause testicular pain, swelling, and, in rare cases, fertility problems. In females, the virus can infect the ovaries, causing oophoritis (inflammation of the ovaries), though this is less commonly observed.
- Central Nervous System (CNS): In rare instances, the mumps virus can cross the blood-brain barrier and infect the central nervous system (CNS). This can lead to a condition known as mumps meningitis or encephalitis, characterized by inflammation of the protective membranes surrounding the brain and spinal cord. CNS involvement can result in symptoms such as headache, neck stiffness, confusion, and even seizures.
🔸Clinical Features:
Incubation period: The time between exposure to the mumps virus and the onset of symptoms is typically around 16-18 days.
▪️Classic Presentation:
♦️Stage 1 or Prodromal stage This refers to the initial phase of mumps infection, lasting for about 3-4 days. During this phase, individuals may experience symptoms such as low-grade fever, malaise, and headache. ♦️Stage 2: The hallmark feature of mumps is inflammation of the salivary glands, particularly the parotid glands, which are located on the sides of the face, in front of the ears. The duration of parotitis is typically at least 2 days, but it can persist for more than 10 days.
Initially, individuals with mumps may present with local tenderness, pain, and earache. Unilateral swelling of the salivary gland, affecting the lateral cheek and jaw area, is commonly observed. As the disease progresses, both salivary glands are usually affected. Redness in the area of the parotid duct and possible protruding ears may also be present. In some cases, a flat, red rash can develop on the face and spread to other parts of the body.
Duration of parotitis: at least 2 days (may persist > 10 days)
Symptoms
May initially present with local tenderness, pain, and earache
Unilateral swelling of the salivary gland (lateral cheek and jaw area); During the course of disease, both salivary glands are usually swollen.
Redness in the area of the parotid duct
Possible protruding ear: The swollen parotid pushes the ipsilateral ear outward and upward.
A flat, red rash that begins on the face and disseminates to the rest of the body can occur.
Chronic courses: Chronic or prolonged courses of mumps are rare.
▪️Subclinical presentation:
In some cases, mumps infection may be subclinical, meaning there are no apparent symptoms. However, even in these cases, individuals can still transmit the virus to others.
It is important to note that about 15-20% of mumps cases can be asymptomatic, meaning individuals may not experience any noticeable symptoms.
🔸Diagnostics
Pathogen detection
Real-time reverse transcriptase PCR (rRT-PCR) on serum or buccal or oral swab
Viral culture (e.g., on CSF, urine, or saliva)
Serology: Positive serum IgM suggests recent infection and confirms the diagnosis.
Relative lymphocytosis
↑ CRP, ↑ ESR
↑ Amylase
🔸Management:
Mumps is usually self-limited with a good prognosis (unless complications arise). Treatment is mainly supportive care.
Medication for pain and fever (e.g., acetaminophen)
Bedrest
Adequate fluid intake
Avoidance of acidic foods and drinks
Ice packs to soothe parotitis
Isolate the patient. [8]
All patients: Isolate for 5 days from the development of parotid swelling.
Hospitalized patients: Initiate droplet precautions.
🔸Complications:
▪️Encephalitis (< 1% of cases)
- Reduced consciousness, seizures
- Neurological deficits: cranial nerve palsy, hemiplegia, sensorineural hearing loss (rare)
▪️Hearing loss (extremely rare)
Classification of Flaviviridae:
Flaviviridae family are part of Enveloped RNA viruses
Classification of Pneumoviridae:
Pneumoviridae family are Enveloped RNA viruses
Classification of Paramyxoviridae:
Paramyxoviridae are Enveloped RNA viruses
Pathogenesis of Yellow Fever:
Yellow fever is called so because it is often associated with jaundice. In severe cases of yellow fever, the virus can cause liver damage, leading to the accumulation of bilirubin in the body. This yellow discoloration gave rise to the name “yellow fever.” It is important to note that not all individuals with yellow fever will develop jaundice, but the name of the disease reflects this common symptom.
🔸Epidemiology:
Yellow fever is endemic in tropical regions of South America and Sub-Saharan Africa.
Asia, Europe, North America, and Australia are free of yellow fever (except for occasional imported cases).
🔸Etiology:
Caused by Yellow fever virus
▪️Transmission:
Yellow fever is primarily transmitted through the bite of infected mosquitoes, specifically the Aedes aegypti species. These mosquitoes become infected with the yellow fever virus when they feed on the blood of an infected person or animal.
- Mosquito acquisition of the virus:
- When an Aedes aegypti mosquito feeds on the blood of an infected person or animal, it takes in the yellow fever virus along with the blood.
- The virus then infects the mosquito’s body, specifically its midgut, where it begins to replicate and multiply.
- Dissemination of the virus within the mosquito:
- As the yellow fever virus continues to replicate, it spreads from the mosquito’s midgut to other organs, including the salivary glands.
- This process typically takes several days.
- Transmission to humans:
- When an infected mosquito bites a human, it injects its saliva into the person’s skin, along with the yellow fever virus if it is infected.
- The virus can then enter the human bloodstream through the mosquito’s saliva, allowing it to spread throughout the body.
- Urban transmission cycle:
- In urban areas where Aedes aegypti mosquitoes are common, the yellow fever virus can be transmitted directly between infected humans and mosquitoes.
- Infected humans serve as a source of the virus for the mosquitoes.
- When an infected mosquito bites another person, it can transmit the virus through its saliva, potentially leading to the spread of yellow fever within the population.
🔸Clinical Features:
Incubation Time:
- The incubation period for yellow fever is typically around 3 to 6 days. This refers to the time between when a person is infected with the virus and when they start experiencing symptoms.
🔸Clinical Features:
- The majority of individuals who are infected with the yellow fever virus do not exhibit any symptoms and remain asymptomatic. However, in symptomatic patients, the disease follows a classic progression in three stages.
▪️ Stage 1 or Period of Infection (3-4 days):
- This stage begins with a sudden onset of high fever, which can reach temperatures as high as 41°C (105°F).
- Headaches and chills are common symptoms during this period.
- Nausea and vomiting may occur, contributing to feelings of general malaise.
▪️ Stage 2 or Period of Remission (up to 2 days):
- After the initial period of infection, there is a temporary easing of symptoms and a decline in fever.
- During this remission period, individuals may experience some relief from their symptoms, and they may feel relatively better.
▪️ Stage 3 or Period of Intoxication (only in approximately 15% of symptomatic patients):
- In some cases, the disease progresses to a more severe stage known as the period of intoxication.
- Hemorrhage, or bleeding, may occur, manifesting as epistaxis (nosebleeds), mucosal bleeding (bleeding from the gums or other mucous membranes), melena (dark, tarry stools), hematuria (blood in the urine), or black vomit.
- Multiorgan dysfunction can occur, leading to conditions such as acute kidney and liver failure.
- Abdominal pain and severe jaundice (yellowing of the skin and eyes) may also be present.
During the Period of Intoxication in yellow fever, approximately 15% of symptomatic patients experience more severe manifestations of the disease. This stage is characterized by two main features: hemorrhage and multiorgan dysfunction.
- Hemorrhage:
- Hemorrhage refers to abnormal bleeding within the body. In yellow fever, it can manifest as various types of bleeding, such as epistaxis (nosebleeds), bleeding from the gums or other mucous membranes (mucosal bleeding), melena (dark, tarry stools), hematuria (blood in the urine), or black vomit.
- The exact mechanism of hemorrhage in yellow fever is not fully understood. However, it is thought to be a result of the virus directly affecting blood vessels, leading to their dysfunction and subsequent bleeding.
- Multiorgan Dysfunction:
- Yellow fever can cause multiorgan dysfunction, particularly affecting the liver and kidneys.
- Liver involvement can result in severe jaundice, where there is a yellowing of the skin and eyes. The virus can directly damage liver cells, leading to liver dysfunction and impaired liver function.
- Kidney involvement can manifest as acute kidney failure, where the kidneys are unable to adequately filter waste products from the blood. This can result in decreased urine output and accumulation of toxins in the body.
The exact mechanisms by which yellow fever leads to multiorgan dysfunction are not fully understood. However, it is believed that the virus directly targets and infects these organs, causing cellular damage and impairing their normal function.
It’s important to note that the Period of Intoxication occurs in a subset of individuals with symptomatic yellow fever, and not all patients progress to this stage. The severity of symptoms and the likelihood of progressing to this stage can vary among individuals.
It’s important to note that not all symptomatic patients progress to the period of intoxication, and the severity of symptoms can vary from person to person. The disease can range from mild cases with flu-like symptoms to severe cases involving organ failure and hemorrhage.
🔸Diagnosis:
▪️Laboratory tests
- ↑ ALT/AST
- Leukopenia
- In period of intoxication: Thrombocytopenia, ↑ PTT
- Signs of organ failure (see acute liver failure, acute renal failure)
▪️Virus detection
- PCR
- ELISA
▪️Liver biopsy
- Used for definitive diagnosis (e.g., postmortem)
- Must not be done while the patient has an active yellow fever infection
- May show Councilman bodies (eosinophilic apoptotic globules). Councilman bodies are apoptosis remnants of hepatocytes.
🔸Management:
- Symptomatic treatment
- No specific antiviral treatment is available
- Avoid NSAIDs that increase the risk of bleeding (e.g., aspirin, ibuprofen, naproxen) in patients with confirmed or suspected yellow fever infection!
Dengue Fever Pathogenesis:
🔸Epidemiology:
Distribution: tropical regions worldwide, particularly Asia (e.g., Thailand)
Incidence
Most common viral disease affecting tourists in tropical regions
🔸Etiology:
- Caused by Dengue virus
▪️Transmission:
Dengue fever is primarily transmitted through the bite of infected mosquitoes, specifically the Aedes aegypti species (These mosquitoes also transmit Yellow Fever virus, Zika virus, and Chikungunya virus). These mosquitoes become infected with the Dengue virus when they feed on the blood of an infected person or animal.
- Mosquito acquisition of the virus:
- When an Aedes aegypti mosquito feeds on the blood of an infected person or animal, it takes in the Dengue virus along with the blood.
- The virus then infects the mosquito’s body, specifically its midgut, where it begins to replicate and multiply.
- Dissemination of the virus within the mosquito:
- As the Dengue virus continues to replicate, it spreads from the mosquito’s midgut to other organs, including the salivary glands.
- This process typically takes several days.
- Transmission to humans:
- When an infected mosquito bites a human, it injects its saliva into the person’s skin, along with the Dengue virus if it is infected.
- The virus can then enter the human bloodstream through the mosquito’s saliva, allowing it to spread throughout the body.
- Urban transmission cycle:
- In urban areas where Aedes aegypti mosquitoes are common, the Dengue virus can be transmitted directly between infected humans and mosquitoes.
- Infected humans serve as a source of the virus for the mosquitoes.
- When an infected mosquito bites another person, it can transmit the virus through its saliva, potentially leading to the spread of yellow fever within the population.
🔸Clinical Features:
Dengue Fever has 3 main clinical entities:
1- Dengue Fever:
The Dengue Fever Classical presentation is the most common and typical presentation. It has 2 subtypes of clinical presentations: Dengue without warning signs and Dengue with warning signs
▪️Dengue without warning signs:
- The incubation period of Dengue Fever is 4-10 days.
- The febrile phase of Dengue Fever is 2-7 days.
🔺 The clinical features of this Subtype includes:
- High fever (40°C) PLUS 2 of the following symptoms during the febrile phase indicate dengue
- Severe headache
- Retro-orbital pain
- Severe arthralgia and myalgia (often referred to as “break-bone fever”)
- Maculopapular, measles-likeexanthem (typically appears 2–5 days after fever onset)
- Generalized lymphadenopathy
- Positive capillary fragility test:
Capillary fragility refers to the susceptibility of small blood vessels called capillaries to rupture or leak. In dengue fever, the dengue virus leads to the activation of the immune system and the release of various substances that affect the integrity of blood vessels.
The capillary fragility test is a simple diagnostic test used to assess the fragility of capillaries. During the test, a blood pressure cuff is placed on the upper arm and inflated to temporarily stop blood flow. After a few minutes, the cuff is released, allowing blood to flow back into the arm. In individuals with normal capillary fragility, no visible signs occur. However, in cases of dengue fever, the capillaries may be more fragile and leaky.
The underlying physiology behind the capillary fragility observed in dengue fever involves the disruption of the endothelial cells that line the capillaries. The dengue virus and the immune response it triggers can cause damage to these cells, leading to increased permeability and fragility of the capillaries. As a result, when blood flow is restored after the cuff is released, the fragile capillaries may rupture or leak, leading to the appearance of small red or purple spots called petechiae on the skin.
Children are usually asymptomatic
▪️Dengue with warning signs:
In dengue fever, the illness progresses through different phases. The critical phase is a period during the course of the disease where there is an increased risk of the patient’s condition worsening. It typically occurs around 3 to 7 days after the onset of symptoms.
During the critical phase, certain changes occur in the body that can lead to more severe symptoms or complications. These changes primarily involve increased vascular permeability, which means that blood vessels become more leaky. This increased permeability can result in the leakage of fluid from blood vessels into tissues, leading to symptoms like plasma leakage, edema, and potentially even organ dysfunction.
Additionally, the critical phase is associated with abnormalities in the clotting mechanisms of the body. This can lead to issues with bleeding and the formation of blood clots in smaller blood vessels.
The timing of the critical phase is often marked by the abatement of fever. As the fever subsides, the risk of clinical deterioration increases. This is why it is important to closely monitor patients during this period for any signs of worsening symptoms or complications.
🔺 Patients at risk of having warning signs during critical phase include:
- Individuals with a history of previous dengue infection
- Infants < 1 year of age
- Patients with severe comorbidities
🔺 Some warning signs that may indicate a worsening condition during the critical phase include:
- Abdominal pain: Severe or persistent abdominal pain can be an indicator of worsening dengue fever.
- Persistent vomiting: Continuous vomiting can lead to dehydration and electrolyte imbalances, which can worsen the overall condition.
- Lethargy or restlessness: Significant changes in energy levels or mental status, such as excessive tiredness or agitation, can suggest worsening symptoms.
- Enlarged liver (> 2 cm): Palpation of an enlarged liver during physical examination can be a sign of liver involvement and potentially severe dengue.
- Signs of fluid accumulation: Pleural effusion (fluid around the lungs) and/or ascites (fluid in the abdominal cavity) can develop during the critical phase, indicating increased vascular permeability and leakage.
- Hemorrhagic manifestations: Petechiae (small red or purple spots on the skin), epistaxis (nosebleeds), and gingival bleeding (bleeding from the gums) are signs of abnormal clotting and increased fragility of blood vessels.
The critical phase is a crucial period where prompt medical intervention is necessary to manage any complications that may arise and prevent further deterioration.
2- Severe Dengue or Dengue Hemorrhagic Fever (DHF):
Severe dengue, also known as dengue hemorrhagic fever (DHF), is a potentially life-threatening form of dengue fever. It occurs as a result of an abnormal immune response in individuals who have been previously infected with one serotype of the dengue virus and are reinfected with a different serotype.
DHF typically occurs as a result of an antibody-dependent reaction in patients who are reinfected with a different serotype
During the initial infection with one serotype of the dengue virus, the immune system produces antibodies to fight off the virus and clear the infection. These antibodies are specific to that particular serotype and can effectively neutralize and eliminate the virus.
However, if a person is later infected with a different serotype of the dengue virus, the antibodies produced during the initial infection may not fully recognize and neutralize the new virus. Instead of effectively eliminating the virus, these antibodies can attach to the new virus particles and form immune complexes.
These immune complexes can then bind to specific immune cells, such as monocytes and macrophages, through receptors on their surface. This binding process is facilitated by the Fc portion of the antibodies in the immune complexes.
The entry of the immune complexes into immune cells can enhance the replication of the virus within these cells. This happens because the immune cells have receptors for the Fc portion of the antibodies, which can facilitate the internalization of the virus into the cell. Once inside the cell, the virus can replicate and cause further damage.
▪️Timing: Severe dengue typically develops around one week after the onset of symptoms, as the initial fever subsides. This distinguishes it from the milder form of dengue fever, in which it occurs after the initial fever subsides.
▪️Incidence: Severe dengue occurs in approximately 1-2% of dengue cases.
▪️Clinical Features of Severe Dengue:
🔺Temperature change: During severe dengue, there may be a temperature change. This can vary from hypothermia, where the body temperature drops below normal, to a second spike in fever.
🔺Hemorrhagic manifestations: One of the key features of severe dengue is thrombocytopenia, which is a decrease in platelet count to less than 100,000/mm3. This can lead to severe hemorrhagic manifestations, such as: - Petechiae - Ecchymoses - Purpura - Hematemesis - Melena (dark, tarry stools)
🔺Severe organ involvement: Severe dengue can affect multiple organs, resulting in significant organ dysfunction.
- Hepatomegaly: During physical examination, an enlarged liver (hepatomegaly) may be observed, indicating liver involvement.
- Liver failure: In severe cases, the liver dysfunction can progress to liver failure, which can have serious consequences.
- Changes in mental status: The dengue virus can affect the central nervous system, leading to changes in mental status such as confusion.
🔺Severely increased vascular permeability: One of the main characteristics of severe dengue is the severe increase in vascular permeability. This means that blood vessels become more leaky, leading to fluid leakage from the blood vessels into surrounding tissues. This can result in various manifestations, such as:
- Pleural effusion: Fluid accumulation around the lungs can cause respiratory distress and difficulty breathing.
- Ascites: Fluid accumulation in the abdominal cavity can lead to abdominal pain and distension.
- Severe changes in hematocrit (Hct): Hematocrit levels, which reflect the proportion of red blood cells in the blood, can be significantly altered in severe dengue. This can result in either an increase (hemoconcentration) or decrease (hemodilution) in hematocrit levels due to fluid shifts.
🔺Positive capillary fragility test
3- Dengue Shock Syndrome (DSS):
Develops due to further deterioration of severe dengue
Presence of both symptoms of severe dengue and circulatory collapse and shock due to plasma leakage
So when Severe dengue + Shock = Dengue Shock Syndrome
🔸Diagnosis:
▪️Laboratory tests
- Leukopenia
- Neutropenia
- Thrombocytopenia
-↑ AST
- Hct significantly increased or decreased in DHF (due to plasma leakage)
▪️Confirmation of diagnosis:
🔺Acute phase (≤ 7 days after symptom onset): - Serologic tests: MAC-ELISA to detect IgM - Molecular Tests (NAAT) to detect viral RNA - NS1 antigen test: detection of the Dengue NS1 antigen (Dengue non-structural protein 1) via ELISA 🔹Allows early detection of the viral antigen in the serum 🔹A positive test confirms the diagnosis (without identifying the dengue serotype) 🔹A negative test does not rule out dengue infection; IgM testing should be performed 🔹Not recommended after day 7 of symptomatic infection (low sensitivity)
- Tissue tests (IHC)🔺Convalescent phase (> 7 days after symptom onset):
- Serologic tests (IgM, IgG)
- Molecular Tests (NAAT)
- Tissue tests (IHC)
🔸Management:
▪️Symptomatic treatment
▪️Fluid administration to avoid dehydration
▪️Acetaminophen
▪️Dengue with warning signs and severe dengue:
- Blood transfusions in case of significant internal bleeding (e.g., epistaxis, gastrointestinal bleeding, or menorrhagia)
- Urgent resuscitation with IV fluids
▪️Avoid NSAIDs that increase the risk of bleeding (e.g., aspirin, ibuprofen, naproxen) in patients with confirmed or suspected Dengue fever infection!
What is the name of the Arthropod that is involved in the transmission of Yellow Fever Virus, Dengue Virus, and Zika Virus:
Aedes aegypti mosquito
Zika Fever Pathogenesis:
🔸Epidemiology:
The Zika virus is mainly found in tropical and subtropical regions. Before 2015, there were only a few reported cases of Zika virus in Africa, southeast Asia, and some Pacific islands.
However, since 2015, there have been epidemic outbreaks of Zika virus in South America, especially in Brazil. During this time, there was a significant increase in the number of people infected with the virus in these areas.
🔸Etiology:
Pathogen: Zika virus
Genus: flavivirus, type of arbovirus
Positive-sense, single-stranded, enveloped RNA
▪️Route of Transmission of Zika Virus:
1. Vector-borne transmission: The most common route of Zika virus transmission is through the bite of infected mosquitoes, primarily the Aedes aegypti mosquito. This mosquito species is known to be a vector for various diseases, including Zika virus, Dengue Virus, Yellow Fever virus, and chikungunya. When a mosquito bites a person who is infected with the Zika virus, it can acquire the virus from the person’s blood. The mosquito can then transmit the virus to another person when it bites them.
2. Transplacental transmission: Another important route of Zika virus transmission is from an infected pregnant woman to her fetus. This is known as transplacental transmission. The virus can cross the placenta and infect the developing fetus, potentially causing a range of birth defects and developmental problems. It is important for pregnant women to take precautions to avoid exposure to the Zika virus, especially in areas where the virus is prevalent.
- Sexual transmission: The Zika virus can also be transmitted through sexual contact. It has been found that the virus can persist in the semen of infected men for an extended period, even months after the initial infection. This means that a man who has been infected with Zika can transmit the virus to his sexual partners, both through vaginal and anal intercourse. It is recommended that individuals practice safe sex or abstain from sexual activity if they have been diagnosed with Zika or have been in an area with active Zika transmission.
Zika virus is the only arbovirus that can also be transmitted sexually.
🔸Clinical Features:
- Incubation Period: 2–14 days
- Approx. 80% of cases remain asymptomatic
- In symptomatic patients, the manifestations are usually mild and last for 2–7 days
- Low-grade fever
- Flu-like symptoms: headache, arthralgia, myalgia, non-purulent conjunctivitis, malaise
- Maculopapular, pruritic rash (20% of cases)
▪️Asymptomatic cases: Approximately 80% of individuals infected with Zika virus do not experience any symptoms. These individuals are considered asymptomatic. Despite not showing any signs of illness, they can still spread the virus to others through mosquito bites or other routes of transmission.
▪️Mild symptoms: In symptomatic patients, the manifestations of Zika virus infection are usually mild. The symptoms typically last for 2 to 7 days. Common symptoms include:
- Low-grade fever: Patients may experience a slight increase in body temperature but not a high fever.
- Flu-like symptoms: Headache, arthralgia (joint pain), myalgia (muscle pain), non-purulent conjunctivitis (redness and irritation of the eyes), and malaise (general feeling of discomfort or unease).
- Maculopapular rash: Around 20% of Zika virus-infected individuals develop a rash, which is characterized by red, raised spots on the skin that are itchy (pruritic). This rash is called maculopapular.
🔸Diagnosis:
▪️Laboratory tests
- Increased Levels of Acute Phase Reactants: Due to acute inflammation there will be increased levels of acute phase reactants.
- Leukopenia: Due to bone marrow suppression and destruction of White blood cells.
- Thrombocytopenia
- Increased LDH (Lactate Dehydrogenase): LDH is an enzyme found in many organs and tissues, including the liver, heart, kidneys, and red blood cells. Elevated LDH levels can indicate cellular damage or inflammation in these organs. In the context of Zika virus infection, increased LDH levels may be a result of tissue damage caused by the virus or an immune response to the infection.
- Increased γ-GT (Gamma-Glutamyl Transferase): γ-GT is an enzyme primarily found in the liver. Elevated γ-GT levels are often associated with liver damage or dysfunction. In the case of Zika virus infection, increased γ-GT levels may indicate liver involvement or inflammation caused by the virus.
▪️Definitive diagnosis
- During the first 7 days of the infection: PCR detects Zika virus RNA in blood and/or urine samples
- During days 7–28: RT-PCR and/or serology
- After 28 days: serology confirms Zika virus antibodies
🔸Management:
▪️Definitive therapy does not yet exist.
▪️Treatment is primarily symptomatic with rest, oral/IV fluids, and/or acetaminophen to relieve fever and pain.
▪️To prevent bleeding, NSAIDs and aspirin should be avoided until dengue has been excluded as a diagnosis.
🔸Complications
▪️Guillain-Barré syndrome (GBS): Zika virus infection has been linked to an increased risk of developing GBS.
▪️Pregnancy related Complications:
🔺Congenital Zika syndrome: When a pregnant woman is infected with Zika virus, the virus can be transmitted to the developing fetus. Congenital Zika syndrome refers to a range of birth defects and developmental abnormalities that can occur in babies exposed to Zika virus during pregnancy. It causes growth restriction and significant CNS complications in neonates resulting from intrauterine transmission of the Zika virus. These can include:
- Microcephaly
- Ventriculomegaly (enlargement of the brain’s fluid-filled spaces)
- Subcortical calcifications (abnormal calcium deposits in the brain)
- Spasticity, hyperreflexia, seizures
- Ocular abnormalities: Zika virus infection can cause ocular abnormalities in newborns, such as pigmentary retinal mottling, which refers to changes in the pigmented layer at the back of the eye.
- Sensorineural hearing loss: Some infants exposed to Zika virus during pregnancy may experience sensorineural hearing loss
🔺Miscarriage: Zika virus infection during pregnancy has also been associated with an increased risk of miscarriage or stillbirth.
What is Congenital Zika syndrome?
🔺Congenital Zika syndrome:
When a pregnant woman is infected with Zika virus, the virus can be transmitted to the developing fetus. Congenital Zika syndrome refers to a range of birth defects and developmental abnormalities that can occur in babies exposed to Zika virus during pregnancy. It causes growth restriction and significant CNS complications in neonates resulting from intrauterine transmission of the Zika virus. These can include:
- Microcephaly
- Ventriculomegaly (enlargement of the brain’s fluid-filled spaces)
- Subcortical calcifications (abnormal calcium deposits in the brain)
- Spasticity, hyperreflexia, seizures
- Ocular abnormalities: Zika virus infection can cause ocular abnormalities in newborns, such as pigmentary retinal mottling, which refers to changes in the pigmented layer at the back of the eye.
- Sensorineural hearing loss: Some infants exposed to Zika virus during pregnancy may experience sensorineural hearing loss.
Pathogenesis of West Nile Fever, Murray Valley encephalitis (MVE), St. Louis encephalitis:
Overview of Acute Upper Respiratory Tract Infections
