MOD 14: Viral Infections Of The CVS And Lymphatics PDF

MICROBIOLOGY AND PARASITOLOGY 11/06/2024. MOD 14: VIRAL INFECTIONS OF THE CVS AND LYMPHATICS...

MICROBIOLOGY AND PARASITOLOGY 11/06/2024. MOD 14: VIRAL INFECTIONS OF THE CVS AND LYMPHATICS Dr. Ma. Teresa A. Barzaga, M.D., FPSP Trans Group/s: 7A, 8A OUTLINE II. MUMPS (EPIDEMIC PAROTITIS) An acute contagious disease characterized by nonsuppurative enlargement of one or both salivary I. Introduction glands. II. Mumps (Epidemic Parotitis) Virus bears morphologic and antigenic characteristics similar to the parainfluenza virus III. Arboviruses Has only one serological type A. Dengue Grows readily in embryonated eggs especially in the B. Yellow Fever (YF) amniotic sac C. Chikungunya Can be grown in cell culture to produce large multinucleated giant cells (syncytia) and a hemagglutinin IV. Rubella Virus A. Transmission Infectivity of virus destroyed by heating at 56C for 20 B. Clinical Manifestations mins Humans are the exclusive natural hosts C. Laboratory Diagnosis Occurs worldwide, epidemics occur in the late winter V. Picornavirus and early spring A. Poliovirus High rate of infection in crowded populations B. Non-Polio Enteroviruses ⅓ of infections are inapparent Most cases occur in children under 15 years ( 40 % VI. Herpesvirus subclinical) A. Cytomegalovirus Lasting immunity follows any form of mumps infection B. Epstein-Barr Virus Mode of transmission: person to person through direct contact with saliva or respiratory droplets from the VII. Filovirus mouth, nose, or throat. A. Ebola Virus ○ An infected person may spread the virus by: Coughing, sneezing, or talking Sharing items that may have saliva (e.g., PART 1 water bottles, cups) Participating in close contact activities (e.g., OBJECTIVES sports, dancing, kissing) Arrive at an accurate etiologic diagnosis based on chief complaint, patient history, and/or preceding A. EPIDEMIOLOGY AND PATHOLOGY OF MUMPS circumstances. Mumps is an acute viral illness that follows a self-limiting Determine the most appropriate clinical specimen, course, but up to 10% of cases have a complicated laboratory tests, and diagnostic procedures. course with involvement of other organ systems Properly identify appropriate management and control ○ Microdeities are reported as complications, but the measures for a given infectious agent. incidence has greatly fallen since the development of the mumps vaccine I. INTRODUCTION Viral pathogens of the circulatory system vary Primary replication occurs in nasal or upper respiratory tremendously both in their virulence and distribution 1 tract epithelial cells worldwide. Some of these pathogens are practically global in their distribution. 2 Viremia The most ubiquitous viruses tend to produce the mildest form of disease, and the majority of cases, Dissemination of virus to salivary glands and other those infected remain asymptomatic. 3 parts of the body (e.g., testes, ovaries. thyroid gland, Other viruses are associated with life-threatening pancreas, meninges, heart, kidney) diseases that have impacted human history. Incubation period : 2-4 weeks followed by symptoms of fever, nasal discharge, muscle pain, and malaise Inflammation of salivary glands (especially the parotids) produce the classic “gopher-like” swelling of the cheeks on one or both sides Prognosis: most will have complete, uncomplicated recovery Microbiology - Mod 14 Viral Infections of the CVS and Lymphatics 1 of 13 The use of trans, practice questions, and evals ratio must be used discreetly and social media/public exposure of the aforementioned shall be strictly prohibited. B. COMPLICATIONS TYPES OF ILLNESSES CAUSED BY ARBOVIRUSES Occurs in 20-50% of young adult The fever and rash is usually a Mild Orchitis and males nonspecific illness resembling other undifferentiated epididymitis Painful but no permanent damage viral illnesses (e.g., influenza and fevers occurs rubella) Virus replicates in beta cells and Eastern equine encephalitis Pancreatitis Severe Western equine encephalitis pancreatic epithelial cells encephalitides St. Louis encephalitis Fever, headache, nausea, Japanese encephalitis vomiting, and stiff neck More common in males Dengue Fever Life-threatening Viral meningitis Appears 2-10 days after onset of Yellow Fever hemorrhagic parotitis Crimean-Congo hemorrhagic fevers Lasts 3-5 days, resolves with few fever or no adverse side effects PATHOGENESIS Rare occurrence (5:100,000 cases) 1 An infected vector bites Affects only one side Hearing loss Virus replicates in the organ of 2 Virus is injected into the capillary circulation Corti causing permanent deafness 3 Viral replication occurs in the vascular endothelium 4 Viremia (precedes onset of clinical symptoms) C. DIAGNOSIS History (exposure) and PE (parotid swelling) Circulating virus reaches the organ for which it has 5 ○ Laboratory studies are not usually required to special tropism establish diagnosis of typical cases Serologic studies Tropism - affinity of a virus for a particular tissue: ○ IgM antibodies by ELISA or 4 fold increase between ○ Liver (yellow fever virus) acute and convalescent sera ○ Brain (encephalitis virus) Viral isolation on monkey kidney cells Arboviruses have a short incubation period of 1 week ○ Samples: saliva, CSF, urine only because the viruses are introduced directly into ○ Timing of collection: within a few days of onset of the bloodstream disease Arboviruses have an associated morbilliform rash, ○ Virus present in saliva for about 1 week after onset secondary to: of parotitis ○ Increased vascular permeability ○ Virus present in urine up to 2 weeks ○ Endothelial cell damage If severe and disseminated, it becomes D. TREATMENT hemorrhagic and involves the mucus Symptomatic treatment usually adequate membranes of the GIT and skin This may lead to Disseminated Intravascular E. PREVENTION Coagulation (DIC), and thrombocytopenia. Live, attenuated mumps vaccine given routinely as part of the MMR vaccine at 15 months of age (powerful and A. DENGUE effective control agent) Also known as break-bone fever Protection often lasts a decade The biggest arbovirus problem in the world today, with the WHO estimating: III. ARBOVIRUSES ○ Between 50 and 100 million cases per year, Viruses spread by arthropod vectors (zoonotic infections This includes 500,000 Dengue hemorrhagic for humans) fever cases, and 22,000 deaths (mostly Transmitted by blood sucking arthropods from one among children) vertebrate host to another Distributed worldwide, but primarily located in tropical The chief vectors regions. Found in Southeast Asia, the Pacific, India, ○ Mosquitos and South America. ○ Ticks Caused by Flavivirus species of four serotypes (Dengue ○ Flies Type 1-4) ○ Gnats Most prevalent flavivirus infection of humans. Vertebrate host : recovers Vector: carries virus for life Important hemorrhagic fevers transmitted by mosquitoes that pose serious threat to humans include: ○ Dengue Fever ○ Yellow Fever ○ Chikungunya Microbiology - Mod 14 Viral Infections of the CVS and Lymphatics 2 of 13 The use of trans, practice questions, and evals ratio must be used discreetly and social media/public exposure of the aforementioned shall be strictly prohibited. 1. PROPERTIES OF DENGUE VIRUSES 3. CLINICAL FEATURES Unstable in the environment, sensitive to: ○ heat 1. Dengue (Breakbone Fever) ○ UV radiation Classically presents with: ○ disinfectants, including alcohol and iodine ○ High fever, Headache ○ acidic pH ○ Maculopapular rash Infections arise from a human-mosquito-human cycle. Scarlatiniform rash may develop within 3-4 Transmitted by Aedes aegypti mosquitoes, which are days. adapted to breed around human dwellings, such as: ○ Lymphadenopathy ○ Man-made water-holding receptacles ○ Myalgia, bone and joint pains ○ Near human habitation Called “Breakbone fever” because myalgia ○ Tree-holes and plants close to human dwellings and deep bone pain are characteristic for DF Epidemics start often during the rainy season when A. Classic dengue fever is self-limited. aegypti is most abundant. Virtually all cases are uncomplicated; deaths are rare. Feeding attempts may number several times a day Begins 4-7 days after a mosquito bite and viremia is depending on the availability of hosts. present at onset of fever, and may persist for 3-5 days. ○ Mosquitoes sheltered indoors bite during the day at ○ Temperature returns to normal after 5-6 days or 1-2 hour intervals in the morning and late afternoon. may subside on the 3rd day and rise again about Viral replication in the mosquito takes 1-2 weeks and 5-8 days after onset. mosquito lifespan is 1-3 months. Dengue fever may be asymptomatic in 80% of infants and children and cannot be distinguished from other 2. PATHOGENESIS common childhood infections as it is just a mild Dengue fever (DF) is primarily a self-limiting disease febrile illness. (usual outcome). ○ Vertical transmission of virus to neonates where Characterized by: mothers had an onset of primary or secondary ○ Abrupt onset of high fever of 40°C (104°F) dengue fever 0-8 days before delivery resulted in ○ Intense headaches acute neonatal dengue fever ○ Rashes More severe in adults with an acute incubation period ○ Slight nose or gum bleeding of 4-7 days with fever, chills, severe frontal headache, ○ Extreme muscle joint & bone pain (AKA Breakbone and retro orbital pain. Fever) Causes the patients to feel as if their bones 2. Dengue Hemorrhagic Fever are breaking Clinical signs are similar to Dengue fever but with As the body temperature returns to normal, some defervescence within 2-7 days. patients may develop signs of Dengue Hemorrhagic Conditions worsen with association of: Fever (DHF): ○ Hypoproteinemia ○ Drowsiness, irritability, severe abdominal pain, ○ Thrombocytopenia severe nose or gum bleeding, persistent vomiting, ○ Prolonged leading time vomiting of blood, black tarry stools. ○ Elevated prothrombin time Patients who developed DHF experience circulatory This may lead to Dengue Shock Syndrome system failure due to increased blood vessel with cyanosis, restlessness, diaphoresis, cool permeability. and clammy skin characterized by shock and Patients with DF can also develop Dengue Shock hemoconcentration. Syndrome (DSS) from vascular collapse because of the Patients with DHF: Circulatory system failure (due to severe drop in blood pressure. INCREASED blood vessel permeability) Patients with DHF/DSS are at greater risk for death Patients with DHF/DSS: Vascular collapse (due to without prompt appropriate supportive treatment. severe DECREASE in blood pressure) ○ Around 30% die among patients with severe DHF may occur in: hemorrhagic disease with poor supportive ○ children with passively acquired maternal antibodies treatment. ○ individuals with preexisting heterologous dengue ○ Mortality can be less than 1% with experienced antibodies due to a previous infection with a support. different serotype of the virus An immunopathological response in some patients, usually in the setting of a heterologous immunity, 3. Dengue Shock Syndrome produces the syndrome DHF-DSS. Shock in DHF-DSS follows sudden extravasation of Cyanosis, restlessness, diaphoresis, and cool, clammy plasma into extravascular sites including pleural and skin abdominal cavities, usually with defervescence of fever. Characterized by shock and hemoconcentration ○ The increased vascular permeability may be due to: Hemorrhagic phenomena and hypovolemic shock due to Increased levels of soluble tumor necrosis increased vascular permeability and plasma leakage factor Patients who develop DF and DHF may experience IFN‐γ circulatory system failure caused by increased blood Activation of the complement system. vessel permeability, as well as vascular collapse because of the severe drop in blood pressure Studies of dengue fever with or without shock in Southeast Asia shows that DSS: ○ Frequently occurs when dengue type 2 is the secondary infecting virus ○ Patient is female, 3 years old or older Microbiology - Mod 14 Viral Infections of the CVS and Lymphatics 3 of 13 The use of trans, practice questions, and evals ratio must be used discreetly and social media/public exposure of the aforementioned shall be strictly prohibited. 4. DIAGNOSIS B. YELLOW FEVER (YF) Caused by a Flavivirus, named from the latin word “flavus,” meaning yellow; only one antigenic type Difficult Restricted to tropical and subtropical areas in Africa, Successful recovery from blood Central and South America, and the Caribbean areas Viral Isolation only before an antibody ○ Once common in the United States and caused response develops several serious outbreaks between 1700-1900, however, this disease has been eliminated in the Identifies the presence of US through vector control efforts. PCR dengue virus and serotypes Transmitted in 2 cycles: Used in specialized labs ○ Urban YF: human to human by the Aedes aegypti Protein-specific capture IgM or mosquito, which is well-adapted to breeding around IgG ELISA human habitations Serology Hemagglutination–Inhibition test ○ Jungle or Sylvatic YF: from infected monkeys to using paired acute and humans by the Haemagogus mosquitoes convalescent serum sample Seen in Africa and South America Man may become incidentally infected while Rapid venturing into jungle areas Detects IgM and IgG Immunochromato High specificity and sensitivity 1. PATHOGENESIS graphic Test Mosquito bite → virus multiplication → spreads to local 5. TREATMENT lymph nodes, liver, spleen, kidney, bone marrow, myocardium Supportive ○ virus present in blood during infection No specific antiviral therapy is available ○ serious disease characterized by hemorrhage and ○ Fluid resuscitation circulatory collapse ○ Normal saline: to maintain circulation ○ virus injury to myocardium may contribute to shock Antipyretics: to relieve symptoms of dengue ○ Aspirin should be avoided to prevent Reye’s 2. CLINICAL MANIFESTATIONS syndrome and hemostatic problems Attentive clinical monitoring of suspected DHF-DSS Most individuals infected with YF have no illness or only cases (e.g. pulse, blood pressure, skin perfusion, urine mild disease with sudden onset of symptoms output, hematocrit) ○ Classically presents with dizziness, chills, fever of ○ Greater than 20% hematocrit increase (e.g. from 39-40C or 102-104F, headache, and generalized 35 to 42%) indicates a significant loss of myalgias. intravascular volume and the urgent need for fluid ○ As symptoms worsen, the face becomes flushed resuscitation and GI complaints (nausea, vomiting, constipation), severe fatigue, restlessness, and irritability are 6. PREVENTION common. ○ Mild disease may resolve after 1-3 days. In endemic areas: mosquito eradication After 3-4 days, the more severely ill patients with a Removal of all containers within premises which may classical YF course will develop bradycardia (Faget’s serve as vessels for egg deposition sign), jaundice, and hemorrhagic manifestations. ○ Relies on public and community based Aedes Approximately 50% of cases progress to moderate to aegypti control programs to remove or destroy severe YF disease mosquito breeding sites, like the Oplan Kiti-Kiti by ○ Fever falls suddenly 2-5 days after onset, but the Department of Health (DOH) reoccurs several hours to days later ○ DOH relaunched the 4 o'clock habit where residents ○ Symptoms of jaundice, petechial rash, mucosal map out high risk areas in a locality, and organized hemorrhages, oliguria or scant urine, epigastric teams to undertake critical response activities tenderness with bloody vomit, confusion, and Insecticidal fogging is considered unhelpful if there are apathy often occur for approximately 7 days no outbreaks ○ After more than a week patients may have a rapid In sealed houses, indoor insecticide sprays should be recovery and no sequelae. effectual 50% of patients with frank YF will develop fatal disease Travelers can protect themselves by using repellants characterized by severe hemorrhagic manifestations, and insecticidal sprays indoors oliguria, and hypotension. Dengvaxia (dengue vaccine by Sanofi) Most severe form is called Malignant Yellow Fever ○ Only beneficial in the prevention of dengue fever to (MYF) those who have already suffered from the other ○ Symptoms: serotypes of the virus Delirium ○ US FDA approved Bleeding ○ DOH statement (January, 2018): Seizures, shock, coma Dengvaxia was “considered defective under Multiple organ failure (in some severe cases, Philippine laws” and suspended the program death) DOH demanded a P1.4 billion refund for the ○ Patients with MYF become immunocompromised cost of the unused vaccine vials and even those in recovery may become DOH asked Sanofi to conduct serotesting of susceptible to bacterial superinfections and the 873,000 children given the vaccine to help pneumonia. determine their pre-vaccination health status ○ Of the 15% of patients who develop moderate/severe disease, up to half may die. ○ Virus injury to myocardium may contribute to shock. Microbiology - Mod 14 Viral Infections of the CVS and Lymphatics 4 of 13 The use of trans, practice questions, and evals ratio must be used discreetly and social media/public exposure of the aforementioned shall be strictly prohibited. 3. DIAGNOSIS ○ After breeding, the eggs can lay dormant for up to one year. Diagnosis is usually based on clinical signs and ○ A carrier mosquito is capable of transmitting the symptoms virus to the next generation. ○ if applicable the patient’s travel history There is no evidence to indicate person-to-person Viral isolation: infection/transmission. ○ From blood during the acute stage ○ Postmortem: from the acidophilic inclusion bodies 1. CLINICAL MANIFESTATIONS seen in the liver Serology: virus specific IgM antibodies (detectable after High fever (similar to dengue fever), joint pain lasting for a week) several months (arthritis), rash, fatigue, headache, Infection can be confirmed through: nausea, vomiting, muscle pain, and blisters. ○ Culture These infections are typically self-limiting and rarely ○ Serology fatal. ○ PCR Postmortem: from acidophilic inclusion bodies in the 2. DIAGNOSIS liver. 1. Presumptive Diagnosis 4. TREATMENT Patient’s clinical features. NO effective treatment Places and dates of travel (from a non-endemic country Supportive care or area) activities. ○ Whenever possible, patient’s with YF should be Epidemiologic history of the location where infection hospitalized for close observation occurred. 5. PREVENTION 2. Laboratory Diagnosis Best method in controlling YF: Viral isolation from patient’s serum during early ○ Surveillance of disease and vector population infections ○ Control of vector by using pesticides through Immunofluorescence elimination of breeding grounds Enzyme immunoassays ○ Personal protection (ex. screening of houses, bed IgG ELISA nets, insect repellants) PCR and RT-PCR Effective method of reducing exposure to Available to detect Chikungunya antigens and patient mosquito vectors antibody response to the infection. Vaccination ○ Live attenuated vaccine 3. Specimen ○ Used for persons living in or traveling to endemic areas Serum or Cerebrospinal Fluid (CSF) ○ Lasts for 10 years ○ In the United States: It is only administered to 4. In Fatal Cases those traveling to areas with endemic yellow fever. Nucleic acid amplification ○ In West Africa: The WHO launched a YF initiative Histopathology with immunohistochemistry in 2006 and since that time, significant progress has Virus culture of biopsy been made in combating YF Autopsy ○ More than 105, 000, 000 people have been vaccinated and no outbreaks of yellow fever were 3. TREATMENT reported in 2015. Supportive care and rest No specific treatment except to manage symptoms with C. CHIKUNGUNYA fluids, analgesics, and bed rest. Transmitted to humans via mosquitoes Aedes aegypti and Aedes albopictus. 4. PREVENTION Belongs to the Alphavirus family. ○ Has a diameter of about 50 nm to 70 nm Best Prevention method: Vector Control ○ Consists of a single stranded positive sense RNA Supportive care and rest ○ Heat sensitive ○ Currently, research initiatives have been taken for Causes several human epidemics in many areas of vaccine development. Africa and Asia and most recently in limited areas of A person suffering from Chikungunya fever should limit Europe. his exposure to mosquito bites to prevent further ○ Until 2013, the disease had not been reported spreading of the infection. outside of Africa, Asia, and a few European Insect repellents containing Picaridin, oil of lemon or countries. However, it has now spread to mosquito eucalyptus populations in North and South America. Wearing long sleeves and pants Mosquitoes have evolved over the years and have ○ Treat the clothes with Permethrin or other repellants effectively adapted themselves for biting humans. Use secure screens on windows and doors to keep ○ While approaching humans, they reduce the mosquitoes out humming of wings and attack from below to Get rid of mosquitoes’ sources in and around the house ensure minimal detection. by emptying standing water from flower pots, buckets, Species of mosquitoes are usually seen in the and barrels. urban areas. Recently they have migrated Change the water in pet dishes and replace the water in mostly to rural areas. bird baths once every week. ○ Aedes mosquitoes need only 2 mL of water for Keep children’s wading pools empty while not in use. breeding. Microbiology - Mod 14 Viral Infections of the CVS and Lymphatics 5 of 13 The use of trans, practice questions, and evals ratio must be used discreetly and social media/public exposure of the aforementioned shall be strictly prohibited.  IV. RUBELLA VIRUS C. LABORATORY DIAGNOSIS Known to cause German Measles Falling rubella antibody titer suggest passively acquired Can cause viral heart infections maternal antibody Link between maternal rubella and certain congenital Rising rubella antibody titer suggests rubella infection defects ○ Can cause serious problems for unborn babies 1. Congenital rubella in the neonatal period whose mothers become infected during pregnancy Antibody to rubella virus should be measured in both infant and maternal A. TRANSMISSION Serial antibody determination in a neonate Droplet infection Rubella IgM in newborn infants serum: transplacental Can occur with subclinical illness infection Transmitted by congenital rubella patients 2. Congenital rubella infection can be diagnosed by B. CLINICAL MANIFESTATIONS Placental biopsy at 12 weeks Adenopathy of the posterior auricular, posterior cervical Demonstration of specific IgM in fetal blood (22 weeks and sub occipital nodes AOG) Maculopapular rash that begins on the face and moves down the body PART 2 1. CONGENITAL RUBELLA SYNDROME V. PICORNAVIRUS Occurs in a developing fetus of a pregnant woman who has contracted rubella PicoRNAviridae THE YOUNGER THE FETUS, THE MORE SEVERE Important family of RNA viruses which include THE ILLNESS poliovirus, coxsackievirus, and echovirus. Non-enveloped, single-stranded RNA viruses (like TIME OF INFECTION DEFECT Caliciviruses) which represent a very large virus family but one of the smallest in terms of virion size and 65-85% chance of either being genetic complexity. First 2 months of spontaneously aborted or gestation developing multiple congenital defects GENUS REPRESENTATIVE 1° DISEASE 30-35% chance of developing a Poliovirus Poliomyelitis 3rd month of fetal life single defect such as deafness (3 serotypes) or congenital heart disease Focal necrosis, Coxsackievirus-A 4th month of 10% risk of a single congenital myositis, (HEV-A) gestation defect Hand-foot-and (21 serotypes) mouth disease Enterovirus Classic Triad for Congenital Rubella Syndrome: Coxsackievirus-B Myocarditis of (HEV-B) 1 Sensorineural deafness newborn (6 serotypes) Eye abnormalities (retinopathy, cataract, glaucoma, Echovirus (HEV-B) Aseptic meningitis, 2 microphthalmia) (28 serotypes) enteritis Congenital heart disease (pulmonary artery stenosis, Enterovirus 72 Hepatitis A 3 patent ductus arteriosus) Rhinovirus Rhinovirus Common Cold 2. RISK OF RUBELLA INFECTION DURING PREGNANCY Encephalo- Cardiovirus Cardiovirus myocarditis PREGNANCY RISK Foot and Mouth Aphthovirus Aphthovirus Preconception Minimal risk Disease 100% risk of fetus being ENTEROVIRUS congenitally infected resulting in major congenital Enteroviruses are so designated because of their ability 0-12 weeks to multiply in the GI tract abnormalities Spontaneous abortion ○ Despite their name, these viruses are not a occurs in 20% of cases prominent cause of gastroenteritis Encompasses more than 115 human serotypes 15% risk of deafness and including enterovirus 68-71 and multiple new 13-16 weeks retinopathy enteroviruses beginning with enterovirus 73 that have been identified by molecular techniques Normal development, slight risk These viruses have no lipid envelopes and are stable in After 16 weeks of deafness and retinopathy acidic environments including the stomach Susceptible to chlorine cleansers but resistant to inactivation by standard disinfectants such as alcohol detergents and can persist for days at room temperature Microbiology - Mod 14 Viral Infections of the CVS and Lymphatics 6 of 13 The use of trans, practice questions, and evals ratio must be used discreetly and social media/public exposure of the aforementioned shall be strictly prohibited. A. POLIOVIRUS TYPES OF POLIOVIRUS INFECTION Causes an acute enteroviral infection of the spinal cord that may cause neuromuscular paralysis After incubation period, about Destruction of motor neurons in the spinal cord 5% of patient present with results in flaccid paralysis minor illness called abortive Most infections are subclinical poliomyelitis, which is Has 3 serotypes: Types 1 and 3 causes the most 1 Mild infection manifested by fever, malaise, severe forms of the disease sore throat, anorexia, myalgia, Portal of entry: Mouth and headache Site of primary multiplication: Oropharynx or intestine This condition usually Protective capsid and lack of an envelope confer resolves in 3 days. chemical stability and resistance to acid and bile detergents Nonparalytic About 1% of patients present ○ Significance: The virus is capable of passing 2 (aseptic with aseptic meningitis or through the gastric environment undamaged, meningitis) nonparalytic poliomyelitis allowing the virus to be pass on to the intestine where it multiplies 3 Paralytic The virus is regularly present in the throat and in the stools before the onset of illness. 4 Progressive postpoliomyelitis muscular atrophy A week after infection, little virus is found in the throat but virus is continuously excreted in the stools for A small number of persons will develop minor several weeks even though high antibody levels are disease (with nonspecific symptoms of fever, headache, present in the blood. nausea, sore throat, and myalgia) Being neurotropic, it may gain access to the CNS via 1. EPIDEMIOLOGY the blood-brain barrier → infiltrate the motor neurons of the spinal cord → invasion of nervous tissue without Infection occurs in all age groups: children are more destruction causes nonparalytic meningitis susceptible Antibodies to poliovirus: occur locally in the In developing countries, these viruses often affect small intestine and tonsils (secretory antibodies) and in the children causing infantile paralysis serum Incidence is more pronounced during the summer Virus neutralizing antibodies form soon after exposure to and fall in temperate zones virus, often before onset of illness and apparently Virus is passed within the population through food, persists for life water, hands, and objects contaminated with feces ○ One exposure confers lifelong immunity Transmission: Mechanical vectors such as flies may occur 3. DIAGNOSIS Polioviruses have been virtually eliminated in North and South America Suspected when epidemics of neuromuscular ○ Its prevalence varies in Asia, Africa, and European disease occurs in the summer in temperate climates countries with infections highest among household Must be differentiated from Guillain-Barre syndrome, contacts. infant botulism, and encephalomyelitis caused by other It can be recovered from pharynx and intestines of enteroviruses patients and healthy carriers The virus can be identified by: Viruses in sewage can serve as a source of contamination of water for drinking, bathing, or irrigation Poliovirus can be isolated by inoculating cell cultures with stool or 2. PATHOPHYSIOLOGY Viral throat washings in the early part of the 1 culture disease Specimens should be kept frozen After ingestion, poliovirus infect epithelial cells in the 1 during transit to the laboratory mucosa of the gastrointestinal tract Polioviruses can also be identified by the Spread or replicate in the submucosal lymphoid tissue 2 PCR 2 Polymerase Chain Reaction (PCR) assays of the tonsils and Peyer’s patches Paired serum samples required to 3 Spread to regional lymph nodes show rise in antibody titer 4 Viremic phase ensues Stage of infection demonstrated by testing serum samples for type and Virus replicates in the organs of reticuloendothelial amount of antibodies 5 Poliovirus can usually be cultured 3-5 system days from blood after infection before 3 Serology development of neutralizing antibodies in some cases, 2nd episode of viremia occurs —> virus While viral replication at secondary replicates further in various tissues sometimes causing sites begins to slow 1 week after symptomatic disease infection, it continues in the ○ Most infections with poliovirus are asymptomatic, gastrointestinal tract. 95% contained as short-term asymptomatic viremia. Poliovirus is shed from the oropharynx for up to 3 weeks after infection and from the GIT as long as 12 weeks. Microbiology - Mod 14 Viral Infections of the CVS and Lymphatics 7 of 13 The use of trans, practice questions, and evals ratio must be used discreetly and social media/public exposure of the aforementioned shall be strictly prohibited. 4. TREATMENT Non-polio enteroviruses can be found in an infected person’s: No specific therapy, treatment rests largely on alleviating ○ Feces/stool pain and suffering ○ Eye, nose, and mouth secretions such as saliva, Respiratory failure may require artificial ventilation nasal mucus or sputum, and blister fluid. Secondary pulmonary infection as a result of impairment One can get exposed to the virus via: of swallowing and coughing may require antibiotics ○ Heavy closed contacts (touching or shaking hands After the acute febrile phase, prompt physical therapy to with an infected person). diminish crippling deformities and to retrain muscles ○ Touching objects or surfaces that have the virus on them. 5. PREVENTION AND CONTROL ○ Changing the diapers of an infected person then Vaccination is the mainstay of prevention touching your eyes, nose, or mouth before washing 2 forms of vaccine currently in use: your hands. ○ Both vaccines are prepared from animal cell ○ Drinking water that has viruses in it. cultures and are trivalent or a combination of three Incidence is highest from late spring to early summer serotypes. in temperate climates ○ Both vaccines are effective. ○ In tropical countries where exposure of infants to 2. MEMBERS OF THE NON-POLIO ENTEROVIRUSES wild viruses is common, both vaccines may be given. 1. Coxsackievirus A Member of the family Picornaviridae, Enterovirus Salk Vaccine Inactivated poliovirus vaccine (IPV) Causes: Sabin Vaccine Oral poliovirus vaccine (OPV) Herpangina Small blister-like bumps or ulcers on Good handwashing practices and the use of gowns and 1 (vesicular the mouth (often at the back of the gloves are important in limiting nosocomial transmission pharyngitis) throat or roof of the mouth). during epidemics. 2 Acute hemorrhagic conjunctivitis Polio immunization must be instituted as early in life as possible, usually four doses starting at about two 3 Aseptic meningitis months of age Quarantine of patients: ineffective because of large Peculiar pattern of lesions on the number of inapparent infections that occur hand, feet, and oral mucosa Immune globulin: of no value after clinical symptoms Hand-foot-and- 4 accompanied by fever, headache, develop mouth disease muscle pain which subsides spontaneously. B. NON-POLIO ENTEROVIRUSES Cause about 10-15 million infections and tens of 2. Coxsackievirus B thousands of hospitalizations each year in the United States. Member of the family Picornaviridae, genus Enterovirus These non-polio enteroviruses are like polioviruses in Mode of Transmission: many epidemiologic and infectious characteristics. Commonly cause transient neonatal infections Fecal-oral route: most common mode Coxsackieviruses A and B, echoviruses, and newer The viruses can spread from person-to-person, enteroviruses are like polioviruses in many 1 usually on an unwashed hands and surfaces epidemiologic and infectious characteristics contaminated by feces 50-80% of enteroviral infections are subclinical and the remainder fall in to the category of “undifferentiated 2 Oral-oral febrile illness Initial phase of infection is intestinal after which the 3 Respiratory droplets virus enters the lymph, blood, and disseminates to other organs Primary multiplication: Oropharynx or intestine Infects the heart, pleura, pancreas, and liver causing 1 Coxsackieviruses A pleurodynia, myocarditis, pericarditis, and hepatitis ○ All coxsackie B viruses are associated with the host 2 Coxsackieviruses B of numerous and various syndromes such as common cold, aseptic meningitis, pleurodynia, 3 Echoviruses pericarditis, myocarditis, upper respiratory illness, pneumonia, and generalized disease of the 4 Enterovirus 72 newborn They are the main viral causes of acute myocarditis 1. TRANSMISSION and pericarditis Most commonly identified causative agent of viral heart disease in humans 1 Oral-fecal Most common cause of myocarditis and are blamed for about ½ of the cases 2 Oral-oral ○ It can cause the flu or attack the heart creating an infection that last for 2-10 days 3 Respiratory droplet Cardiac symptoms can potentially occur within 2 weeks and doesn’t usually cause death but may cause permanent heart damage particularly if it recurs Microbiology - Mod 14 Viral Infections of the CVS and Lymphatics 8 of 13 The use of trans, practice questions, and evals ratio must be used discreetly and social media/public exposure of the aforementioned shall be strictly prohibited. 3. CLINICAL MANIFESTATION VI. HERPESVIRUS Pleurodynia (“devil’s grip”), an acute disease characterized by recurrent, sharp, sudden intercostal or A. CYTOMEGALOVIRUS abdominal pain accompanied by fever and sore throat Also known as Human Herpesvirus 5 ○ Recovery is spontaneous and complete Member of the Herpesvirus Aseptic meningitis High infection rates in the human population Severe Generalized Disease of infants It is currently estimated that 50% of people in the United Adults males: Myocarditis and pericarditis States have been infected by the time they reached ○ Seen principally in adult males and are important as adulthood it can be mistaken with myocardial infarction 60% of the population eventually become infected; in ○ Prognosis is good and complete recovery is the rule some developing countries, the figure is up to 95% ○ There is evidence for persistent infection linked with A major cause of non-Epstein Barr Virus Infectious chronic myocarditis and chronic dilated Mononucleosis in the general human population cardiomyopathy An important pathogen in immunocompromised hosts Infants: viral myocarditis (may be rapid in onset and including patients with AIDS, neonates, and transplant fatal) recipients ○ Coxsackie B are the most common cause of Primary infection is usually asymptomatic; the virus then viral myocarditis in infants and it may be rapid in becomes latent and is reactivated from time to time. onset and fatal ○ Spread of the virus to the heart in infants can cause 1. TRANSMISSION: extensive damage to the myocardium, leading to Can be transmitted between individuals through contact heart failure and death in nearly half of the cases with body fluids, such as saliva or urine. ○ Heart involvement in older children and adults are Common modes of transmission (require intimate generally less serious contact) include: Many viral heart infections create no visible symptoms, the infection can go unnoticed 1 Sexual contact Symptoms include the following: 2 Vaginal birth Abnormal heartbeat Muscle aches 3 Transplacental Chest pain Sore throat 4 Nursing Fatigue Joint/Leg pain or swelling 5 Blood transfusion Fever Fainting/Shortness of breath 6 Organ transplantation 4. DIAGNOSIS Congenital cytomegalovirus infections Pregnant women with active infections frequently Virus Isolation: Throat washings and Stool pass this virus to their fetus, resulting in congenital cytomegalovirus infections, which occur in 7 1 Throat Washings (during the first few days of illness) approximately 1 in 150 infants in the United States. ○ Infants can also be infected during passage 2 Stool (during the first few weeks of illness) through the birth canal or through breast milk and saliva from the mother. Methods for the Direct Detection of Enteroviruses Provide rapid and sensitive assays useful for clinical 2. EPIDEMIOLOGY samples. Nucleic acid detection (RT PCR) Among the most ubiquitous pathogens of humans ○ Reverse transcription polymerase chain reaction Although not noted to be highly communicable, appears tests can be broadly reactive to detect many to be transmitted in: serotypes ○ Neutralizing antibodies: 1 Saliva Appear early during the course of infection Tend to be specific for the infecting virus 2 Milk Persists for years Serology 3 Urine ○ Other methods such as immunofluorescence 4 Respiratory mucus 5. TREATMENT 5 Semen There are no vaccines or antiviral drugs currently available for prevention or treatment. 6 Cervical secretions Symptomatic treatment is given 7 Feces 6. PREVENTION 8 Lymphocytes Basic Sanitation on the part of Food Service Workers Handwashing: is the best protection ○ Care should be taken in washing one's hands. ○ Remind everyone in the family to wash their hands well, especially after using the toilet, before meals, and before preparing food. Microbiology - Mod 14 Viral Infections of the CVS and Lymphatics 9 of 13 The use of trans, practice questions, and evals ratio must be used discreetly and social media/public exposure of the aforementioned shall be strictly prohibited. 3. INFECTION AND DISEASE Other inclusion disease: Most healthy adults and children are asymptomatic Chorioretinitis and optic Vast majority of cytomegalovirus infections are 1 Eye atrophy asymptomatic In adults, if symptoms do occur, they typically include: 2 Ear Sensorineural deafness Hepatosplenomegaly and 1 Fever 3 Liver jaundice which is due to 2 Fatigue hepatitis 3 Swollen glands 4 Lung Pneumonitis 4 Pharyngitis 5 Heart Myocarditis 6 Thrombocytopenia, purpura, haemolytic anemia More virulent form of disease develops in: Late sequelae in individuals Hearing defects and reduced 1 Fetuses 7 asymptomatic at intelligence 2 Newborn birth 3 Immunodeficient adults Clinical features: Some symptoms include: 1 Intrauterine growth retardation 2 Jaundice 1 Hepatomegaly 3 Thrombocytopenia 2 Splenomegaly 4 Hepatosplenomegaly 3 Jaundice 5 Microcephaly 4 Capillary bleeding 6 Retinitis 5 Microcephaly 7 Myocarditis 6 Ocular inflammation These features manifest if the virus crosses the placenta Severe, extensive damage may cause death within during the embryonic state when the body systems are days or weeks developing in utero. Babies who survive develop long-term neurologic However, 80% of infected infants will never have sequelae (hearing/visual defects) symptoms or experience long-term problems Mortality rates are about 10% 4. CYTOMEGALIC INCLUSION DISEASE OF NEWBORN 5. DIAGNOSIS Most common congenital viral infection Characterized by involvement of the central nervous system and the reticuloendothelial system Cultivation of Still the method for detecting Defined as the isolation of CMV from the saliva or urine 1 the saliva or Cytomegalovirus in newborn within 3 weeks of birth virus from urine babies up to three weeks CNS abnormalities: For typical cell enlargement and Tissue 2 prominent inclusions in cytoplasm 1 Microcephaly examination and nucleus (not specific) 2 Mental retardation IgM from the blood of the neonate: 3 Spasticity indicates current infection 4 Epilepsy IgG from the blood of the neonate: 3 Serological tests indicates past infection 5 Periventricular calcification Unreliable in the immunocompromised Isolation of the CMV from the urine or saliva of the neonate 4 Viral culture Takes long (2-3 weeks) Has replaced virus isolation routine 5 PCR detection of infection Microbiology - Mod 14 Viral Infections of the CVS and Lymphatics 10 of 13 The use of trans, practice questions, and evals ratio must be used discreetly and social media/public exposure of the aforementioned shall be strictly prohibited. 6. TREATMENT 3. DISEASES Drugs recently approved: ganciclovir, foscarnet, When uninfected young adults are exposed to the EBV, hyperimmune CMV Ig they may experience infectious mononucleosis Interferon not helpful Virus is mainly spread by contact of bodily fluids (e.g. saliva, blood, semen) 7. CONTROL 1. Infectious Mononucleosi