INDEX

Preface.

Introduction.

PART a

Viruses: Common Characteristics.

1. Virus: Sendai RNA virus. (SeV), (SEND)
2. Virus: Rous RNA sarcoma. (RSV)
3. Virus: Adenovirus. DNA (MAV-1, MAD-1&2, FAV-1 to 8, TAV-1 & 2)
4. Virus: Cytomegalovirus. (CMV, MCMV, HHV-5, HCMV)
5. Virus: Encephalomyocarditis. -- RNA. (EMCV, TBEV)
6. Virus: Ectromelia, the DNA poxvirus of mice. (ECTV)
7. Virus: HI (Toolan) virus. (THV)
8. Virus: Sialodacryoadenitis coronavirus. RNA (SDAV)
9. Virus: Hantavirus. RNA - (HFRS, KHF, EHF, NE)
10. Virus: Coronaviruses. RNA (RCV, SDAV, PRC, IBV, MERS-COV, HCoV-, SARS-COV)

    PART b

11. Virus: Avian leukosis. (ALV/ALV-J) retrovirus
12. Virus: Rotaviruses. RNA (EDIM, ADRV, CAL) - gastroenteritis
13. Virus: Lymphocytic choriomeningitis. RNA (LCMV)
14. Virus: Theiler's encephalomyelitis. RNA (TMEV, GD VII, SAFV, VHEV)
15. Virus: Kilham rat parvovirus. DNA (RV, KRV, RPV-1, RPV-2, MKV)
16. Virus: Newcastle disease. RNA (NDV)
17. Virus: Anellovirus. DNA (TTV, TTMV, TMDV, PRA, SAV, SealAV, ZcAV)
18. Virus: Mouse Minute Parvovirus. DNA (MVM(p), MVM(i), RV, PVR-1)
19. Virus: Polyoma virus. DNA (MPV, BKV, JCV, SV40, PyV, RPV, BFD ..)
20. Virus: Norovirus. RNA (NoV, SRSVs)

PART c

• Virus: Chickenpox, varicella zoster virus (VZV)
• Virus: Hepatitis -- Liver inflammation -- 5 viruses.
• Virus: Measles, Morbilliviruses, RNA (MV, RPV)
• Virus: Reovirus type 3. RNA (ARV, MRV, BRV, NBV, RRV, )
• Virus: Pneumonia, DNA/RNS - Influenza, Syncytial, Parainfluenza. (RSV, PIV, )

PART d

Parasite: Chlamydial intracellular bacterial virus.

Bacteria: Tularemia -- Intracellular bacterium.

- Virus : Murine retroviruses. DNA (MuLV, HIV.., SMRV, MoMLV, HTLV, BLV)

- Virus : Quailpox Virus, DNA (AVP, )

Parasite: Borrelia (Deer/Bear tick)

-Focus-: Monographs on Toxins and Enhancers.

Virus: Chickenpox, varicella zoster virus (VZV) INDEX
https://en.wikipedia.org/wiki/Chickenpox, 2015-12-16

LINK 2:http://emedicine.medscape.com/article/1131785-overview, 2015-02-10
LINK 3: http://umm.edu/health/medical/ency/articles/chickenpox, 2015
LINK 4: http://dermatology.about.com/cs/../chickencomp.htm, 2014-12-16
LINK 5: http://dermatology.about.com/cs/../chickentreat.htm, 2014-12-29
LINK 6: http://dermatology.about.com/cs/../chickenpreg.htm, 2014-12-11
LINK 7: http://www.bhchp.org/..Manual/.../Varicella..pdf, 2013, Homeless
LINK 8: http://chickenpox.emedtv.com/../chickenpox-p2.html, 2013-06-04, TV
LINK 9: ..//healthland.time.com/../5-things..-chickenpox-and-shingles/, 2013-01-29
LINK 10: http://www.bop.gov/news/PDFs/varicella.pdf, 2013, Prisons
LINK 11: http://virology-online.com/viruses/VZV3.htm, 2008
LINK 12: http://www.rcog.org.uk/.../GT13ChickenpoxinPregnancy2007.pdf

Chickenpox, also known as varicella, is a highly contagious disease caused by the initial infection with varicella zoster virus (VZV), an enveloped virus. The disease results in a characteristic skin rash that forms small, itchy blisters, which eventually scab over.[2] It usually starts on the chest, back, and face then spreads to the rest of the body.[2] Other symptoms may include fever, feeling tired, and headaches.[2] Symptoms usually last five to ten days.[2] Complications may occasionally include pneumonia, inflammation of the brain, or bacterial infections of the skin among others.[3] The disease is often more severe in adults than children.[4] Symptoms begin ten to twenty one days after exposure to the virus.[5]

Chickenpox is an airborne disease which spreads easily through the coughs and sneezes of an infected person.[5] It may be spread from one to two days before the rash appears until all lesions have crusted over.[5] It may also spread through contact with the blisters.[5] Those with shingles may spread chickenpox to those who are not immune through contact with the blisters.[5] The disease can usually be diagnosed based on the presenting symptom;[6] however, in unusual cases may be confirmed by polymerase chain reaction (PCR) testing of the blister fluid or scabs.[4] Testing for antibodies may be done to determine if a person is or is not immune.[4] People usually only get the disease once.

Exposure to VZV in a healthy child initiates the production of host immunoglobulin G (IgG), immunoglobulin M (IgM), and immunoglobulin A (IgA) antibodies; IgG antibodies persist for life and confer immunity. Cell-mediated immune responses are also important in limiting the scope and the duration of primary varicella infection. After primary infection, VZV is hypothesized to spread from mucosal and epidermal lesions to local sensory nerves. VZV then remains latent in the dorsal ganglion cells of the sensory nerves. Reactivation of VZV results in the clinically distinct syndrome of herpes zoster (i.e., shingles), postherpetic neuralgia,[25] and sometimes Ramsay Hunt syndrome type II.[26] Varicella zoster can affect the arteries in the neck and head, producing stroke, either during childhood, or after a latency period of many years.

After a chickenpox infection, the virus remains dormant in the body's nerve tissues. The immune system keeps the virus at bay, but later in life, usually as an adult, it can be reactivated and cause a different form of the viral infection called shingles (also known as herpes zoster).[28] The United States Advisory Committee on Immunization Practices (ACIP) suggests that every adult over the age of 60 years get the herpes zoster vaccine.[29]

Shingles affects one in five adults infected with chickenpox as children, especially those who are immune suppressed, particularly from cancer, HIV, or other conditions. Stress can bring on shingles as well, although scientists are still researching the connection.[30] Shingles are most commonly found in adults over the age of 60 who were diagnosed with chickenpox when they were under the age of 1.

Secondary bacterial infection of skin lesions, manifesting as impetigo, cellulitis, and erysipelas, is the most common complication in healthy children. Disseminated primary varicella infection usually seen in the immunocompromised may have high morbidity. Ninety percent of cases of varicella pneumonia occur in the adult population. Rarer complications of disseminated chickenpox include myocarditis, hepatitis, and glomerulonephritis

The early (prodromal) symptoms in adolescents and adults are nausea, loss of appetite, aching muscles, and headache. This is followed by the characteristic rash or oral sores, malaise, and a low-grade fever that signal the presence of the disease. Oral manifestations of the disease (enanthem) not uncommonly may precede the external rash (exanthem). In children the illness is not usually preceded by prodromal symptoms, and the first sign is the rash or the spots in the oral cavity. The rash begins as small red dots on the face, scalp, torso, upper arms and legs; progressing over 10\u201312 hours to small bumps, blisters and pustules; followed by umbilication and the formation of scabs.[12][13]

At the blister stage, intense itching is usually present. Blisters may also occur on the palms, soles, and genital area. Commonly, visible evidence of the disease develops in the oral cavity and tonsil areas in the form of small ulcers which can be painful or itchy or both; this enanthem (internal rash) can precede the exanthem (external rash) by 1 to 3 days or can be concurrent. These symptoms of chickenpox appear 10 to 21 days after exposure to a contagious person. Adults may have a more widespread rash and longer fever, and they are more likely to experience complications, such as varicella pneumonia.[12]

Because watery nasal discharge containing live virus usually precedes both exanthem (external rash) and enanthem (oral ulcers) by 1 to 2 days, the infected person actually becomes contagious one to two days before recognition of the disease. Contagiousness persists until all vesicular lesions have become dry crusts (scabs), which usually entails four or five days, by which time nasal shedding of live virus ceases.

The condition usually resolves by itself within a couple of weeks.[14] The rash may, however, last for up to one month, although the infectious stage does not last longer than a week or two.

Chickenpox occurs in all parts of the world.[4] Before routine immunization the number of cases occurring each year was similar to the number of people born.[4] Since immunization the number of infections in the United States has decreased nearly 90%.[4] In 2013 chickenpox resulted in 7,000 deaths globally \u2013 down from 8,900 in 1990.[10] Death occurs in about 1 per 60,000 cases.[4] Chickenpox was not separated from smallpox until the late 19th century.[4] In 1888 its connection to shingles was determined.[4] The first documented use of the term chicken pox was in 1658.[11] Various explanations have been suggested for the use of "chicken" in the name, one being the relative mildness of the disease.

During pregnancy the dangers to the fetus associated with a primary VZV infection are greater in the first six months. In the third trimester, the mother is more likely to have severe symptoms.[16] For pregnant women, antibodies produced as a result of immunization or previous infection are transferred via the placenta to the fetus.[17] Women who are immune to chickenpox cannot become infected and do not need to be concerned about it for themselves or their infant during pregnancy.[18] Varicella infection in pregnant women could lead to spread via the placenta and infection of the fetus. If infection occurs during the first 28 weeks of gestation, this can lead to fetal varicella syndrome (also known as congenital varicella syndrome).[19] Effects on the fetus can range in severity from underdeveloped toes and fingers to severe anal and bladder malformation. Possible problems include:

• Damage to brain: encephalitis,[20] microcephaly, hydrocephaly,[21] aplasia of brain

• Damage to the eye: optic stalk, optic cup, and lens vesicles, microphthalmia, cataracts, chorioretinitis, optic atrophy

• Other neurological disorder: damage to cervical and lumbosacral spinal cord, motor/sensory deficits, absent deep tendon reflexes, anisocoria/Horner's syndrome

• Damage to body: hypoplasia of upper/lower extremities, anal and bladder sphincter dysfunction

• Skin disorders: (cicatricial) skin lesions, hypopigmentation

Infection late in gestation or immediately following birth is referred to as "neonatal varicella".[22] Maternal infection is associated with premature delivery. The risk of the baby developing the disease is greatest following exposure to infection in the period 7 days before delivery and up to 8 days following the birth. The baby may also be exposed to the virus via infectious siblings or other contacts, but this is of less concern if the mother is immune. Newborns who develop symptoms are at a high risk of pneumonia and other serious complications of the disease.

Treatment:
Because chicken pox is usually a benign self-limited disease, treatment is typically aimed at treating symptoms and making the patient more comfortable. In some cases, the antiviral medication acyclovir may be used to treat chicken pox.

Acetaminophen
Patients with chicken pox typically have viral-type, prodromal symptoms such as headache, fever, fatigue, and muscle aches. These symptoms can be treated with acetaminophen (Tylenol) with doses determined by the weight of the patient. Children should never be given aspirin or medications containing aspirin for chicken pox or any other viral illness because of the risk of Reye's syndrome.

Soothing Baths
Frequent baths are sometimes helpful to relieve itching.
Adding finely-ground (colloidal) oatmeal such as Aveeno can help improve itching.
Oatmeal baths can be prepared at home also by grinding or blending dry oatmeal into a fine powder and adding about 2 cups to the bath water. One-half to one cup of baking soda may also be added to bath water to reduce itching.

Lotions
The most common lotion used for chicken pox is Calamine lotion.
This or any similar over-the-counter preparation can be applied to the blisters to help dry them out and soothe the skin.

Antihistamines
Over-the-counter and prescription antihistamines may be used to control severe itching.
Diphenhydramine (Benadryl) is available over-the-counter and hydroxyzine (Atarax) is available by prescription. Both of these antihistamines cause drowsiness and may be helpful at night to help the patient sleep. The newer antihistamines such as loratadine (Claritin), certrizine (Zyrtec), and fexofenadine (Allegra) can be used to control itching but do not cause drowsiness.

Preventing Scratching
Scratching increases the risk of secondary bacterial infections.
All patients with chicken pox should have their nails trimmed short.
In addition, small children may have to wear mittens to reduce scratching.

Acyclovir
Acyclovir (Zovirax) is an anti-viral drug that may be used to treat chicken pox.
In uncomplicated cases acyclovir taken 5 times a day has been shown to cause shorter periods of new lesion formation, fewer lesions, and more rapid healing but only if started within 24 to 48 hours of the onset of the rash. Acyclovir has not been shown to decrease the rate of complications in otherwise healthy children who get chicken pox. Oral acyclovir is more strongly recommended for children with underlying skin disease such as eczema, newborns, adults, and smokers since this group is at greater risk for complications. IV acyclovir is used for people with compromised immune systems.

Other Anti-Virals
Currently acyclovir (Zovirax) is the only FDA-approved treatment for chicken pox.
... the antiviral medications valacyclovir (Valtrex) used to treat herpes simplex virus infections, has been shown to be effective for chicken pox and are often prescribed.

Chicken pox is usually a benign, self-limited, viral infection caused by the varicella virus. However, chicken pox acquired during pregnancy causes an increase risk of complications to the mother and the infant. The time of infection, during early pregnancy or near delivery, determines the risk to mother and child.

Pregnant women who have a history of a previous chicken pox infection or who have been immunized have antibodies to the virus. These antibodies are transferred to the infant through the placenta throughout the pregnancy. Therefore, pregnant women who are immune and are exposed to someone with chicken pox do not need to worry about complications for themselves or their infant.

Testing for Immunity in Pregnancy
All women should be questioned about previous chicken pox infection or immunization at their first prenatal visit. Of those women who do not remember a past infection or immunization, 80% to 90% have antibodies and are considered immune. For this reason, testing for antibodies is controversial, but many practitioners obtain this test at the first prenatal visit.

Maternal Complications of Chicken Pox in Pregnancy
A primary chicken pox infection occurs in only 0.05% to 0.07% of pregnancies because most women of childbearing age have immunity to the varicella virus because of a previous infection or immunization. Women who do acquire chicken pox while pregnant, especially in the third trimester, are at a greater risk of developing varicella pneumonia. Varicella pneumonia is a potentially life-threatening infection of the lungs by the varicella virus.

Infant Complications of Chicken Pox in Early Pregnancy
Primary chicken pox infection in the first trimester of pregnancy, especially weeks 8 to 12, carries a 2.2% risk of congenital varicella syndrome, a syndrome of birth defects in the infant. The most common manifestation of congenital varicella syndrome is scarring of the skin.

Cough During Pregnancy
Other abnormalities that can occur include a smaller than normal head, eye problems, low birth weight, small limbs, and mental retardation.

Infant Complications of Chicken Pox in Late Pregnancy
If a woman acquires a primary chicken pox infection within 5 days before and 2 days after delivery, her newborn is at risk for disseminated varicella infection. Disseminated varicella infection occurs when the virus infects a newborn before the transfer of protective maternal antibodies. This overwhelming viral infection leads to death in 25% of cases.

Treatment of Pregnant Women with Chicken Pox
Women who acquire primary chicken pox during pregnancy should be treated with the antiviral drug acyclovir (Zovirax) which seems to be safe in pregnancy. Pregnant women with varicella pneumonia should be treated with IV acyclovir and be observed in the hospital. In addition women who are not immune to varicella, but are exposed may be treated with varicella-zoster immunoglobulin (VZIG), a substance that triggers an immune response against the varicella virus.

Treatment of Infants with Chicken Pox
Infants whose mothers develop varicella 5 days before delivery or 2 days following delivery should receive VZIG after birth. Infants who develop varicella during the first 2 weeks of life should be treated with IV acyclovir.

Prevention.
Stay away from people!
The spread of chickenpox can be prevented by isolating affected individuals.
Contagion is by exposure to respiratory droplets, or direct contact with lesions, within a period lasting from three days before the onset of the rash, to four days after the onset of the rash.[32] The chickenpox virus is susceptible to disinfectants, notably chlorine bleach (i.e., sodium hypochlorite). Like all enveloped viruses, it is sensitive to desiccation, heat and detergents.

Virus: Hepatitis -- Liver inflammation -- 5 viruses. INDEX
https://en.wikipedia.org/wiki/Viral_hepatitis (2015-07-16)

LINK 02: http://www.cdc.gov/hepatitis/abc/index.htm (2015-06-16)
LINK 03: http://emedicine.medscape.com/../775507-overview (2014-12-16)
LINK 04: http://hepatitis.about.com/../ViralHepatitis.htm (2014-11-24)
LINK 05: http://www.medicinenet.com/viral_hepatitis/.. (2014-01-10)
LINK 06: ..//www.womenshealth.gov/.../viral-hepatitis.html (2012-07-06)
LINK 07: ..//www.microbiologybook.org/../hepatitis-virus.htm (2011-05-24)
LINK 08: https://www.ncbi.nlm.nih.gov/pubmed/21279280 (2011-01-10)
LINK 09: http://www.scielo.cl/.../v138n10/art%2016.pdf (2010-10)
LINK 10: http://www.criver.com/...mouse_hepatitis_virus.aspx (2009)
LINK 11: http://dora.missouri.edu/../mouse-hepatitis-virus-mhv/
LINK 12: http://www.zoologix.com/.../MouseHepatitis.htm
LINK 13: https://www.newscientist.com/..mouse-hepatitis-virus...
LINK 14: https://en.wikipedia.org/wiki/Mouse_hepatitis_virus
LINK 15: ..//www.niddk.nih.gov/.../ViralHepatitis...pdf (2012-04-23)

The classic hepatotropic viruses, hepatitis A through E, are not the only viral agents able to infect the liver. Other systemic viruses may cause hepatic injury that can range from mild and transient elevation of aminotransferases to acute hepatitis and occasionally acute liver failure and fulminant hepatitis. The clinical presentation may be indistinguishable from that associated with classic hepatotropic viruses.

These agents include
• cytomegalovirus;
• Epstein-Barr virus;
• herpes simplex virus;
• varicella-zoster virus;
• human herpesvirus 6, 7, and 8;
• human parvovirus B19;
• adenoviruses
• .. others.

Cytomegalovirus:
Wide spectrums of clinical syndromes are associated with cytomegalovirus disease.
Unique clinical syndromes may present in neonates, young adults and immunocompromised hosts infected with cytomegalovirus.

Epstein Barr virus: Cases of fulminant hepatitis have been reported in both immunocompromised and immunocompetent hosts infected with Epstein Barr virus. Occasionally, these patients with acute hepatic failure may need liver transplantation.

Herpes simplex viruses may involve the liver in neonatal infections, pregnancy, immunocompromised hosts and occasionally, immunocompetent adults.

Varicella-Zoster virus has also been associated with severe acute hepatitis and fulminant hepatitis in adults.

Human herpesviruses 6, 7, and 8, human parvovirus B19, and adenoviruses can also be present with features of acute liver injury and occasionally as fulminant hepatitis. The clinical syndromes are less well delineated than those associated with herpesviruses.

The drug of choice for these conditions is intravenous acyclovir.
These may also need liver transplantation in the more severe forms of clinical presentation.

Typical liver biopsy findings can be useful in determining the diagnosis of these viral infections.

It is important to consider these viruses as possible etiologic agents in patients who have acute liver injury and their serologic markers for the classic hepatotropic viruses are not indicative of an active infection.

Virus: Measles, Morbilliviruses, RNA (MV, MeV, RPV) INDEX
https://en.wikipedia.org/wiki/Measles (2015-11-25)

LINK 02: http://jgv.microbiologyresearch.org/content/journal/jgv/... 2015-12-08
LINK 03: ..//well.blogs.nytimes.com/..susceptibility-to-other-infections/ (2015-05-07)
LINK 04: http://www.sciencemag.org/content/348/6235/694 (2015-05-08)
LINK 05: https://www.ncbi.nlm.nih.gov/pubmed/25294240 (2015-01)
LINK 06: http://qjmed.oxfordjournals.org/.../177.full.pdf (2014-05-27)
LINK 07: ..www.thanhniennews.com/../vietnam-..calls-for-calm...423.html (2014-04-18)
LINK 08: http://www.ncbi.nlm.nih.gov/../1743-422X-7-52.pdf (2010-03-04)

LINK 09: http://news.bbc.co.uk/2/hi/south_asia/4987406.stm (2006-05-16)
LINK 10: https://www.ncbi.nlm.nih.gov/pubmed/14998696 (2004-04)
LINK 11: https://www.ncbi.nlm.nih.gov/pubmed/12022432 (2002-04)
LINK 12: http://www.microbiologyresearch.org/..medmicro-44-3-231b.pdf (1996-03)
LINK 13: http://jgv.microbiologyresearch.org/../0022-1317-67-9-1971 (1986-09)
LINK 14: http://jgv.microbiologyresearch.org/../0022-1317-64-6-1205 (1983-06)
LINK 15: http://www.microbiologyresearch.org/../mic-34-2-285.pdf (1963-07)
LINK 16: https://www.ncbi.nlm.nih.gov/.../archdisch01512-0040.pdf (1931)

Measles is caused by the measles virus (MV), a single-stranded, negative-sense, double-layered enveloped RNA virus of the genus Morbillivirus within the family Paramyxoviridae. It is also known as morbilli, rubeola or red measles. The virus was first isolated in 1954.

It is a highly contagious infection caused by the measles virus.
Initial signs and symptoms typically include fever, often greater than 40 °C (104.0 °F), cough, runny nose, and red eyes. Two or three days after the start of symptoms, small white spots may form inside the mouth, known as Koplik's spots. A red, flat rash which usually starts on the face and then spreads to the rest of the body typically begins 3 to 5 days after the start of symptoms. Symptoms usually develop 10-12 days after exposure to an infected person and last 7-10 days. Complications occur in about 30% and may include diarrhea, blindness, inflammation of the brain, and pneumonia among others. Rubella (German measles) and roseola are different diseases.

Measles is an airborne disease which spreads easily through the coughs and sneezes of those infected.
It may also be spread through contact with saliva or nasal secretions. Nine out of ten people who are not immune who share living space with an infected person will catch it. People are infectious to others from 4 days before to 4 days after the start of the rash. People usually do not get the disease more than once.

The identification of poliovirus receptor-like 4 (PVRL4) as the second natural receptor for measles virus (MV) has closed a major gap in our understanding of measles pathogenesis, and explains how this predominantly lymphotropic virus breaks through epithelial barriers to transmit to a susceptible host. ... mild/self-limiting nature of the infection. ... the use of two cellular receptors, CD150 and PVRL4, governs the in vivo tissue-specific temporal patterns of virus spread and resulting pathological lesions. ...

The virus initially infects dendritic cells in the alveoli.
These cells drain into nearby lymph nodes and infect lymphocytes leading to viral replication.
Infected cells circulate in the blood and spread around the body delivering the virus to organs such as the skin, lung, liver, spleen and brain. After an incubation period of 6-19 days, prodromal symptoms develop, including a stepwise increase in fever to around 39C or higher, cough, coryza, conjunctivitis and a cluster of white lesions on the buccal mucosa known as Koplik spots that are pathognomonic for measles. Two to four days after the prodrome, a cell-mediated reaction involving T-helper cells releasing interferon a and interleukin-2 leads to the formation of a morbilliform rash characteristically beginning on the face and head and spreading to cover the whole body. The rash remains for 5-36 days and then fades in the order it appeared.

Encephalitis is an inflammation of the brain parenchyma and typically manifests with a triad of symptoms comprising fever, headache and altered level of consciousness. Other symptoms include disorientation, behavioural and speech disturbances and neurological signs such as hemiparesis and seizures.

(2010) The measles virus emerged from rinderpest (Cattle Plague) as a zoonotic disease between 1100 and 1200 AD.

(1986) The data exclude the presence of small intervening genes between the six major genes of morbilliviruses and indicate the gene order to be the same as that proposed for Sendai virus (and Newcastle disease virus) and different from that of simian virus 5. ... The virions appear to contain six proteins analogous to those of paramyxoviruses. These have been designated the L, H, P, N, F and M proteins. ... the possible role of the N protein in regulation of transcription and replication. ... The role of the M protein in persistent infection ... the key role of this protein in assembly and budding.

Encephalitis is the most frequent neurological complication of measles virus infection.
... four types of measles-induced encephalitis including primary measles encephalitis, acute post-measles encephalitis, measles inclusion body encephalitis and subacute sclerosing panencephalitis. The early symptoms of encephalitis may be non-specific and can be mistakenly attributed to a systemic infection leading to a delay in diagnosis.

Common symptoms of encephalitis such as fever and altered level of consciousness are not specific for encephalitis ....

(1996) In developing countries it is estimated that there are 50 million cases of measles annually, resulting in almost a million deaths. The morbidity associated with measles is also great; it potentiates the effects of diarrhoea disease and other respiratory pathogens. ... (AND) Measles remains a major problem in developing countries, where it affects an estimated 30 million children a year and causes up to one million deaths annually. It resulted in about 96,000 deaths in 2013, down from 545,000 deaths in 1990.

In 1980, the disease is estimated to have caused 2.6 million deaths per year. The risk of death among those infected is usually 0.2%, but may be up to 10% in those who have malnutrition. Between 1987 and 2000, the case fatality rate across the United States was three measles-attributable deaths per 1000 cases, or 0.3%. In underdeveloped nations with high rates of malnutrition and poor healthcare, fatality rates have been as high as 28%. In immunocompromised persons the fatality rate is approximately 30%.

Measles blindness is the single leading cause of blindness among children in low income countries, accounting for an estimated 15,000 to 60,000 cases of blindness per year. There is a close synergism between measles and vitamin A deficiency that can result in xerophthalmia, with corneal ulceration, keratomalacia, and subsequent corneal scarring or phthisis bulbi. High-dose oral vitamin A supplementation is recommended for all children with measles in developing countries. Higher measles immunization coverage to interrupt measles transmission and interventions aimed at improving vitamin A nutriture of children are the main (current) strategies to prevent measles blindness.

(1983) The study of proteins in the virions of the morbilliviruses such as measles virus (MV), canine distemper (CDV), rinderpest (RPV) and peste-des-petits ruminants (PPR) viruses and proteins induced by these viruses in infected cells has been stimulated greatly over the past 5 years because of the involvement of these viruses in chronic diseases in their natural hosts (Appel et al., 1981). MV has been associated with acute and subacute sclerosing panencephalitis (SSPE) and CDV induces chronic distemper encephalitis and old dog encephalitis (ODE).

SYMPTOMS:
The classic signs and symptoms of measles include 4-day fevers (the 4 D's) and the 3 C's -- cough, coryza (head cold, fever, sneezing), and conjunctivitis (red eyes) -- along with fever and rashes. Fever is common and typically lasts for about 1 week; the fever seen with measles is often as high as 40 °C (104 °F). Koplik's spots seen inside the mouth are pathognomonic (diagnostic) for measles, but are temporary and therefore rarely seen. Recognizing these spots before a person reaches their maximum infectiousness can help physicians reduce the spread of the disease.

The characteristic measles rash is classically described as a generalized red maculopapular rash that begins several days after the fever starts. It starts on the back of the ears and, after a few hours, spreads to the head and neck before spreading to cover most of the body, often causing itching. The measles rash appears two to four days after the initial symptoms and lasts for up to eight days. The rash is said to "stain", changing color from red to dark brown, before disappearing.[13] Overall, the disease from infection with the measles virus usually resolves after about three weeks.

Immunosuppression after measles is known to predispose people to opportunistic infections for a period of several weeks to months. Using population-level data, we show that measles has a more prolonged effect on host resistance, extending over 2 to 3 years. We find that nonmeasles infectious disease mortality in high-income countries is tightly coupled to measles incidence at this lag, in both the pre- and post-vaccine eras. ... long-term immunologic sequelae of measles drive interannual fluctuations in nonmeasles deaths.

That measles depresses the immune response has been known for some time.
Animal studies suggest that measles infection depletes B and T lymphocytes, specialized white blood cells that produce antibodies that "remember" the measles virus, providing immunity against further attacks.

The immune system then recovers, but for many months after, the cells that repopulate the system are almost all effective only against the measles virus. You will never get measles again, but you are temporarily left susceptible to other diseases.

"it seems that when measles was prevalent, it would go through a population, and that population would be at increased risk for mortality from other diseases for about 28 months, and in proportion to how many people were infected with measles."

"The immune system is working fine," Dr. Mina explained.
"But the assortment of stuff it protects against is decreased.
Kids have to get re-exposed to other diseases to gain immunity to them."

"It's the absence of measles that is driving down mortality from other diseases,"

Activation of the innate immune response represents one of the most important cellular mechanisms to limit virus replication and spread in cell culture. ... adenoviral gene expression on the antiviral response in adenovirus-transformed cell lines, i.e. HEK293, HEK293SF, and AGE1.HN. ...the expression of the early region protein 1A (E1A) in these cell lines impairs their ability to activate antiviral genes by the interferon pathway. This property may help in the isolation of newly emerging viruses and the propagation of interferon-sensitive virus strains.

1931 -- The steady decline in the virtulence of diphtheria acnd scarlet fever which has been in progress during the (1900s) has thrown into sharper prominence the continued severity and fatality of measles. Taking epidemic and non-epidenic years together, measles is responsible for 08 per cent. of (deaths from all causes in (the UK), aand imust be held responsible for much chronic ill-health, as a result of its pulmonary complications. In average epidemics all but a negligible proportion of the deaths occur within the first 5 years of life in communities in which measles is endemic. ... With regard to the prognosis in any given case, the factor of age is so well known that little remains to be said on this score, though it is perhaps worth while to mention that the low mortality among adults only holds for communities in which measles is widespread throughout the child population.

On the average, about four-fifths of measles deaths are directly attributable to pneumonia in one form or another, broncho-pneumonia of a severe type being responsible, as is well known, for the greatest number.

The case mortality among cases treated in hospitals appears to be so gravely in excess of that observed in those which are left at home, that the argument is sometimes advanced that no attempt should be made to accumulate cases of measles in large institutions, on account of the dangerous infectivity of measles pneumonia under the over-crowded conditions which are likely to exist in hospital wards during epidemics. ... measles can be safely nursed in general wards provided that the density of beds is kept within proper limits. A minimum of 144 square feet of floor space per bed shouild be maintained.

... a common sequence of events in measles might be the same as that so frequently noted in influenza; first bronchial infection with B. influenze, then pneumonia due to the pneumococcus, followed at a later stage by necrosis and suppuration produced by hemolytic streptococci. ... In many respects measles bears a close resemblance to influenza, especially as regards the pathology and bacteriology of the complications.

Vitamin A does have a beneficial effect on morbidity associated with measles and (could) be used as a treatment for hospitalized measles cases. A total of 492 children, aged from 6 months to 13 years, were supplemented with vitamin A, and 536 children were given placebo in 6 trials, 5 of which were conducted in hospitals and one in a community setting. The main outcome measures were: incidence of pneumonia, diarrhoea, croup, and otitis media; and duration of pneumonia, diarrhoea, fever and hospitalization.

There was no significant reduction in the incidence of pneumonia or diarrhoea but there was a 47 per cent reduction in the incidence of croup in children who were treated with 200 000 IU of vitamin A on 2 consecutive days. ... one study reported a 74 per cent reduction in the incidence of otitis media. There was a statistically significant decrease in the duration of diarrhoea, pneumonia, hospital stay and fever in individual studies.

There is no specific treatment for measles.
Most people with uncomplicated measles will recover with rest and supportive treatment.

Patients who become sicker may be developing medical complications.
Some people will develop pneumonia as a consequence of infection with the measles virus.
Other complications include ear infections, bronchitis (either viral bronchitis or secondary bacterial bronchitis), and brain inflammation. Brain inflammation from measles has a mortality rate of 15%. While there is no specific treatment for brain inflammation from measles, antibiotics are required for bacterial pneumonia, sinusitis, and bronchitis that can follow measles.

All other treatment addresses symptoms, with ibuprofen or paracetamol to reduce fever and pain and, if required, a fast-acting medication to dilate the airways for cough. As for aspirin, some research has suggested a correlation between children who take aspirin and the development of Reye syndrome. Some research has shown aspirin may not be the only medication associated with Reye, and even antiemetics have been implicated.

Even in countries where vaccination has been introduced, rates may remain high.
Measles is a leading cause of vaccine-preventable childhood mortality. Worldwide, the fatality rate has been significantly reduced by a vaccination campaign led by partners in the Measles Initiative: the American Red Cross, the United States' Centers for Disease Control and Prevention (CDC), the United Nations Foundation, UNICEF and the WHO. Globally, measles fell 60% from an estimated 873,000 deaths in 1999 to 345,000 in 2005. Estimates for 2008 indicate deaths fell further to 164,000 globally, with 77% of the remaining measles deaths in 2008 occurring within the Southeast Asian region.

(2015) Dr. (Michael J. Mina) Mina, now a medical student at Emory University, said that the measles vaccine has provided a significant added benefit in addition to protecting against measles. After the vaccine came into use, rates of both measles and non-measles infections dropped. The reduction in measles cases after the vaccine was introduced is the main reason for the reduction in rates of other infectious diseases.

"It's the absence of measles that is driving down mortality from other diseases," he said.

In industrialized countries, it is mainly deaths from respiratory infections that are prevented by the vaccine; in poor countries, the vaccine primarily reduces deaths from diarrheal diseases and dysentery. The effect has been significant, driving childhood infectious disease deaths in Western countries down to six per 100,000 after the vaccine from 16 per 100,000 before.

Researchers examined data on post-measles infections in the United States, England and Wales, and Denmark both before and after the measles vaccine became available in the 1960s. They found a correlation between the number of measles cases in a given period and the number of deaths from non-measles infectious diseases in children in the two to three years afterward.

"With mathematical analysis of all of the epidemiological evidence we have," said the lead author, Michael J. Mina, who was a postdoctoral researcher at Princeton when the study was done, "it seems that when measles was prevalent, it would go through a population, and that population would be at increased risk for mortality from other diseases for about 28 months, and in proportion to how many people were infected with measles."

Measles is an endemic disease, meaning it has been continually present in a community, and many people develop resistance. In populations not exposed to measles, exposure to the new disease can be devastating. In 1529, a measles outbreak in Cuba killed two-thirds of those natives who had previously survived smallpox. Two years later, measles was responsible for the deaths of half the population of Honduras, and it had ravaged Mexico, Central America, and the Inca civilization.

Between roughly 1855 and 2005, measles has been estimated to have killed about 200 million people worldwide. Measles killed 20 percent of Hawaii's population in the 1850s. In 1875, measles killed over 40,000 Fijians, approximately one-third of the population. In the 19th century, the disease killed 50% of the Andamanese population. Seven to eight million children are thought to have died from measles each year before the vaccine was introduced.

The local authorities in the Andamans (islands off the coast of India) have been criticised by environmentalists and non governmental organisations for not taking enough steps to protect the tribes and preserve their habitat. In 2006, nearly 50 children and several adults from an isolated tribe in India's Andaman and Nicobar Islands contracted measles. Doctors said that unless controlled, the illness could seriously affect the Jarawa tribe which once numbered 5,000 and was then down to about 270 people. Initially officials said that the Jarawas were only affected by "heat rash".

In the 19th century, measles killed at least half of the Great Andamanese on one island and all those on another, said Survival International, which campaigns for tribal groups. When 108 Jarawas contracted measles in 1999, the authorities first denied the existence of the outbreak, but later were forced to concede the illness existed after testimony from doctors on the islands, Survival International said. Later in 2006, doctors said that many of the ill had been admitted to the Pant Government Hospital in Port Blair, capital of the Andaman and Nicobar Islands.

"That tribe, also once 5,000-strong, now numbers only 41 people."

Virus: Reovirus type 3. RNA (ARV, MRV, BRV, NBV, RRV, ) INDEX
http://emedicine.medscape.com/article/227348-overview (2015)

LINK 02: https://en.wikipedia.org/wiki/Reoviridae (2015-11-03)
LINK 03: http://www.zoologix.com/.../Reovirus3.htm
LINK 04: http://emedicine.medscape.com/../300455-overview (2015-01-13)
LINK 05: http://viralzone.expasy.org/all_by_species/105.html (2015)
LINK 06: ..//www.criver.com/../infectious-agents/..reovirus.aspx (2009)
LINK 07: http://emedicine.medscape.com/...clinical (2014-12-17)
LINK 08: http://www.sciencedirect.com/.../0042682288905557 (1988)
LINK 09: http://www.jpeds.com/.../S0022-3476.../pdf (1984-12)
LINK 10: http://www.pnas.org/../857.full.pdf (1965-06-30)
LINK 11: http://jvi.asm.org/content/61/5/1407.abstract (1987-05)
LINK 12: http://www.jstor.org/../25437...tab_contents (1984)
LINK 13: https://www.nlm.nih.gov/.../000073.htm (2015-11-02)

Viruses in the family Reoviridae have genomes consisting of segmented, double-stranded RNA (dsRNA).
Reoviruses are non-enveloped and have an icosahedral capsid composed of an outer (T=13) and inner (T=2) protein shell. The genomes of viruses in Reoviridae contain 10-12 segments which are grouped into three categories corresponding to their size: L (large), M (medium) and S (small). Segments range from about 3.9 to 1 kbp and each segment encodes 1-3 proteins (10-14 proteins in total). Reoviridae proteins are denoted by the Greek character corresponding to the segment it was translated from (the L segment encodes for b proteins, the M segment encodes for c proteins and the S segment encodes for c3 proteins).

Replication occurs exclusively in the cytoplasm and the virus encodes several proteins which are needed for replication and conversion of the dsRNA genome into (+)-RNAs. The virus can enter the host cell via a receptor on the cell surface. The receptor is not known but is thought to include sialic acid and junctional adhesion molecules (JAMs). The virus is partially uncoated by proteases in the endolysosome, where the capsid is partially digested to allow further cell entry. The core particle then enters the cytoplasm by a yet unknown process where the genome is transcribed conservatively causing an excess of (+) sense strands, which are used as mRNA templates to synthesize sense strands. Viral particles begin to assemble in the cytoplasm 6-7 hours after infection. Translation takes place by leaky scanning, suppression of termination, and ribosomal skipping. The virus exits the host cell by monopartite non-tubule guided viral movement, cell to cell movement, and existing in occlusion bodies after cell death and remaining infectious until finding another host.

Reoviridae is a family of viruses.
They have a wide host range, including vertebrates, invertebrates, plants, and fungi.
There are currently 87 species in this family, divided among 30 genera. The family Reoviridae is divided into 9 genera, 4 of which -- Orthoreovirus, Coltivirus, Rotavirus, and Orbivirus -- can infect humans and animals. Four other genera infect only plants and insects, and one infects fish. Although almost 100 orbivirus serotypes are known, only 3 serotypes of orthoreovirus and 2 of coltivirus have been identified. The genus Rotavirus contains 3 groups, A, B, and C, with group A causing most outbreaks of disease. Both orthoreoviruses and orbiviruses contain 10 segments of double-stranded RNA. Rotaviruses contain 11 genome segments, and coltiviruses have 12 segments.

Reoviruses can affect the gastrointestinal system (such as Rotavirus) and respiratory tract.
The name "Reo-" is derived from Respiratory Enteric Orphan viruses.
The term "orphan virus" refers to the fact that some of these viruses have been observed not associated with any known disease. Even though viruses in the Reoviridae family have more recently been identified with various diseases, the original name is still used.

The dsRNA genome is never completely uncoated, to prevent activation of antiviral state by the cell in response to dsRNA. The viral polymerase lambda3 synthesizes a capped and non-polyadenylated monocistronic mRNA from each dsRNA segment. These capped mRNAs are translocated to the cell cytoplasm where they are translated.

Reovirus infection occurs often in humans, but most cases are mild or subclinical.
Rotavirus, however, can cause severe diarrhea and intestinal distress in children.
The virus can be readily detected in feces, and may also be recovered from pharyngeal or nasal secretions, urine, cerebrospinal fluid, and blood. Despite the ease of finding Reovirus in clinical specimens, their role in human disease or treatment is still uncertain.

Some viruses of this family infect plants. For example, Phytoreovirus and Oryzavirus.

The reoviruses have been demonstrated to have oncolytic (cancer-killing) properties, encouraging the development of reovirus-based therapies for cancer treatment.

Virus: Pneumonia, DNA/RNS - Influenza, Syncytial, Parainfluenza.
-- (RSV, PIV-1, PIV-2, PIV-3, JCV, BKV, SARS, MERS, HTLV-1, HSV-1 to HSV-8, VZV, CMV ) INDEX
https://en.wikipedia.org/wiki/Viral_pneumonia (2015-11-03)

LINK 02: http://emedicine.medscape.com/../300455-overview (2015-01-13)
LINK 03: https://www.nlm.nih.gov/medlineplus/../000073.htm (2015-11-02)
LINK 04: http://www.zoologix.com/.../PneumoniaVirusOfMice.htm
LINK 05: http://www.zoologix.com/.../StreptococcusPneumoniae.htm
LINK 06: http://www.criver.com/../..pneumonia_virus_of_mice.aspx
LINK 07: ..//www.pneumoniasymptoms.org/../viral-pneumonia.html (2006)
LINK 08: http://radiopaedia.org/articles/neonatal-pneumonia

VIRAL Pneumomia is fundamentally a destruction of lung and bronchial tissues by the influence of one, or more, of a number of viruses. Often, one of these virus infections can lead to a state of pneumonia. Sometimes, more than one virus may be involved. Frequently, the health and immune weakening influence of the viral load will encourge, allow, or, invite a bacterial infection which will then further encourage the symptoms of pneumonia, and, make a diagnosis relevant for optimal medical support very difficult. Viral pneumonias that manifest as a rash include varicella-zoster virus (chickenpox) and measles virus.

Diagnostic errors can be costly.
Attempting to treat a viral or a bacterial infection when the reality is the alternative may only permit further health decline. Treating only either the viral or the bacterial, when it is a combination, will only delay an effective and optimal improvement. In some cases, the prescription of a drug of particular benefit only to a virus which is not present, as a misinterpretation of or projection of what the virus is, will not only delay recovery but may accelate the disease state.

Viruses account for the largest proportion of childhood pneumonia.
Viral pneumonia decreases in frequency in healthy young and middle-aged adults, but it then increases substantially among the elderly. Studies on community-acquired pneumonias consistently demonstrate viruses to be the second most common etiologic cause (behind Streptococcus pneumoniae), ranging from 13-50% of diagnosed cases.

Viral pneumonia is a subset of the pneumonitides, which were at one time called atypical pneumonias.
In the past, all pneumonias were labeled atypical if a bacterial pathogen could not be identified with Gram staining and if the pneumonia did not respond to antibiotics. Many viral pneumonias have overlapping clinical presentations with each other and with bacterial pneumonia -- and may occur together with bacterial pneumonia -- making diagnosis on purely clinical grounds difficult or impossible. An accurate and early etiologic diagnosis is important because specific therapies are used against certain viruses. Even with currently available tests, however, in some series a causative microorganism could not be identified in 50-80% of symptomatic patients.

Severity:
Depending on the virulence of the organism, as well as the age and comorbidities of the patient, viral pneumonia can vary from a mild and self-limited illness to a life-threatening disease.

The common constitutional symptoms of viral pneumonia:
Fever
Chills
Nonproductive cough
Rhinitis
Myalgias
Headaches
Fatigue

During physical examination, the patient may also display the following:
Tachypnea and/or dyspnea
Tachycardia or bradycardia
Wheezing
Rhonchi
Rales
Sternal or intercostal retractions
Dullness to percussion
Decreased breath sounds
Pleurisy
Pleural friction rub
Cyanosis
Rash
Acute respiratory distress

Influenza pneumonia
The influenza viruses are the most common viral cause of pneumonia.
Primary influenza pneumonia manifests with persistent symptoms of cough, sore throat, headache, myalgia, and malaise for more than three to five days. The symptoms may worsen with time, and new respiratory signs and symptoms, such as dyspnea and cyanosis, appear.

Infection by influenza virus leads to cell death, especially in the upper airway.
When direct viral infection of lung parenchyma occurs, hemorrhage is seen along with a relative lack of inflammatory cells. Mucociliary clearance is impaired, and bacterial adherence to respiratory epithelium occurs.

Infection with the influenza virus impairs T lymphocytes, neutrophil, and macrophage function, which leads to impairment of host defenses and may foster bacterial infection of normally sterile areas, including the lower respiratory tract. This impairment of host defenses may explain why as many as 53% of outpatients with bacterial pneumonia have a concurrent viral infection.

Respiratory syncytial virus pneumonia (RSV)
Respiratory syncytial virus (RSV) is the most frequent cause of lower respiratory tract infection in infants and children and the second most common viral cause of pneumonia in adults. Patients with RSV pneumonia typically present with fever, nonproductive cough, otalgia, anorexia, and dyspnea. Wheezes, rales, and rhonchi are common physical findings.

Parainfluenza virus pneumonia, types A and B. (PIV-1, PIV-2, PIV-3)
Parainfluenza virus (PIV) is second in importance only to RSV as a cause of lower respiratory tract disease in children and pneumonia and bronchiolitis in infants younger than 6 months. PIV pneumonia and bronchiolitis are caused primarily by the PIV-3 strain. The signs and symptoms include fever, cough, coryza, dyspnea with rales, and wheezing.

Both DNA and RNA viruses are involved in the etiology of viral pneumonia. Some are well-known lung pathogens that produce common clinical and radiologic manifestations. Others are rarely involved as lung pathogens.

Etiologic viruses include various families, as follows:

Adenoviridae ( adenoviruses)
Coronaviridae (coronaviruses) - SARS, MERS
Bunyaviridae (arboviruses) - Hantavirus
Orthomyxoviridae (orthomyxoviruses) - Influenza virus
Papovaviridae (polyomavirus) -- JC virus, BK virus
Paramyxoviridae (paramyxoviruses) - Parainfluenza virus (PIV), respiratory syncytial
virus (RSV), human metapneumovirus (hMPV), measles virus
Picornaviridae (picornaviruses)
  -- Enteroviruses, coxsackievirus, echovirus, enterovirus 71, rhinovirus
Reoviridae ( rotavirus)
Retroviridae (retroviruses) -- Human immunodeficiency virus (HIV), 
                            human lymphotropic virus type 1 (HTLV-1)

Most of the members of Herpesviridae family are documented lung pathogens in hosts with compromised cell immunity and include the following:

Herpes simplex virus 1 (HSV-1) and herpes simplex virus 2 (HSV-2), 
also called human herpesvirus 1 (HHV-1) and human herpesvirus 2 (HHV-2), respectively
Herpesvirus 6, herpesvirus 7, and herpesvirus 8
Varicella-zoster virus (VZV)
Cytomegalovirus (CMV)
Epstein-Barr virus (EBV)

Influenza virus, respiratory syncytial virus, adenovirus, parainfluenza virus, coronavirus, rhinovirus, and human metapneumovirus may cause community-acquired viral pneumonia.

Specific treatments for the various types of viral pneumonia include the following:

Influenza pneumonia:
Amantadine hydrochloride and rimantadine hydrochloride are approved for the prevention and treatment of influenza A virus infection. Their efficacy in patients with influenza viral pneumonia or severe influenza is unknown.

RSV pneumonia:
Ribavirin is the only effective antiviral agent available for the treatment of RSV pneumonia, but there are conflicting data regarding its efficacy.

PIV pneumonia:
Treatment is mainly supportive, but aerosolized and oral ribavirin have been associated with reduction in PIV shedding and clinical improvement in immunocompromised patients.

After contamination, most respiratory viruses tend to multiply in the epithelium of the upper airway and secondarily infect the lung by means of airway secretions or hematogenous spread. Severe pneumonias may result in extensive consolidation of the lungs with varying degrees of hemorrhage. Some patients developed bloody pleural effusions and diffuse alveolar damage. The mechanism of damage to tissues depends on the virus involved. Some viruses are mainly cytopathic, directly affecting the pneumocytes or the bronchial cells. With others, overexuberant inflammation from the immune response is the mainstay of the pathogenic process.

Immune responses can be categorized according to patterns of cytokine production.
Type 1 cytokines promote cell-mediated immunity, while type 2 cytokines mediate allergic responses.
Children infected with respiratory syncytial virus (RSV) who develop acute bronchiolitis, rather than mild upper respiratory infection symptoms, have impaired type 1 immunity or augmented type 2 immunity.

In addition to humoral responses, cell-mediated immunity appears to be important for recovery from certain respiratory viral infections. Impaired type 1 response may explain why immunocompromised patients have more severe viral pneumonias.

Respiratory viruses damage the respiratory tract and stimulate the host to release multiple humoral factors, including histamine, leukotriene C4, and virus-specific immunoglobulin E in RSV infection and bradykinin, interleukin 1, interleukin 6, and interleukin 8 in rhinovirus infections. RSV infections can also alter bacterial colonization patterns, increase bacterial adherence to respiratory epithelium, reduce mucociliary clearance, and alter bacterial phagocytosis by host cells.

Viral pneumonia may leave patients with residual disability from interstitial fibrosis.
Infants hospitalized with lower lung infection due to RSV are much more likely to later develop asthma.

The US census for 2000-2001 listed pneumonia/influenza as the seventh leading cause of death (down from sixth) despite a 7.2% decrease in the mortality rate for these diseases during this period. Severe influenza seasons can result in more than 40,000 excess deaths and more than 200,000 hospitalizations.

Patients aged 65 years or older are at particular risk for death from viral pneumonia as well as from influenza not complicated by pneumonia. Deaths in these patients account for 89% of all pneumonia and/or influenza deaths.

Morbidity, especially in elderly persons, is also high.
Up to 10-12% of patients older than 65 years required a higher level of assistance for activities of daily living after hospitalization for acute respiratory illnesses. In one nursing home outbreak, residents with acute influenza illness showed significant functional decline.

Agents used in cases of viral pneumonia include acyclovir, ganciclovir, and immunoglobulin.

In cases of viral pneumonia where influenza A or B are thought to be causative agents, patients who are seen within 48 hours of symptom onset may benefit from treatment with oseltamivir or zanamivir.

Respiratory syncytial virus (RSV) may be treated with ribavirin.

Herpes simplex virus and varicella-zoster virus infections are usually treated with aciclovir.

Cytomegalovirus is usually treated with ganciclovir.

There is no known (2015) efficacious treatment for pneumonia caused by SARS coronavirus, adenovirus, hantavirus, parainfluenza or H1N1 virus; treatment is largely supportive.

INDEX