A presentation on serious viral infections covering epidemology, clinical features and managment, with images of manifestations. Focus is mainly on Emergency department presentation

1. Serious
Viral
Infections
Dr Raseena Vattamkandathil
MEM Resident

2. INFLUENZA

3. ❏ Highly infectious
❏ Transmitted via aerosolized
respiratory secretions, large droplets,
or fomites.
❏ Peaking in the winter months of
temperate climates
❏ Mortality occurs mostly among the
elderly and young infants.

4. ❏ Antigenic drift in their surface antigens that allow the virus to re-infect
individuals and reemerge each winter.
❏ Major antigenic changes that increase population susceptibility and lead to a
pandemic.

5. ❏ Mortality during pandemics occurs more frequently among
healthy adults
❏ Seasonal influenza  those at the extremes of age are more
likely to die

6. Clinical features of influenza
❏ Abrupt onset of fever and respiratory symptoms.
❏ Most cases are self-limited
❏ Elderly, the very young, and those with comorbid conditions, might require
hospitalization
❏ Exacerbations of chronic medical conditions, such as CCF or COPD

7. Diagnosis
❏ Delirium is common in the elderly.
❏ Pneumonia complicates some influenza infections.  can progress to ARDS
often within 24 hours
Most cases of influenza are diagnosed clinically when a patient presents with
fever, aches, and cough with influenza virus circulating in the community

8. When to go for lab confirmation? Before influenza
emergence is clear

9. …….Diagnosis
Rapid antigen assays
 Identify the surface proteins in influenza A and B  give results within 15
minutes.
 Low sensitivity (10% - 80%) and high Specificity( 90% -95%) ie a positive
test indicates high likelihood of influenza during an outbreak.
PCR
 More sensitive and specific than antigen tests.
 Best used in patients hospitalized with suspected influenza.

10. Treatment of influenza
 The majority have a self-limited illness requiring only symptomatic care.
 Patients with more severe influenza
● IV fluids
● respiratory support
● vasopressors (if signs of shock exist)

11.  Treat patients with pneumonia with antibiotics, targeting MRSA if severe
pneumonia exists.
 Extracorporeal membrane oxygenation aids those with severe cardiorespiratory
dysfunction, especially in pandemic settings when younger patients are
afflicted.

12. Spanish flu(1980- 1920)
American Expeditionary Force flu patients at U.S. Army Camp
Hospital no. 45 in Aix-les-Bains, France, 1918 Soldiers sick with Spanish flu at a hospital ward, Camp Funston, Fort
Riley, Kansas.
estimated 500 million people, had been infected in four successive waves. Estimates of deaths range from 17 million to 50 million,[7]
and possibly as high as 100 million, making it one of the deadliest pandemics in history.

13. Neuraminidase inhibitors (Oseltamivir)
 Limited roles in otherwise healthy adults and children
 The CDC recommends treating higher-risk populations.
 In healthy patients outside extremes of age a modest benefit if the patient starts
therapy within 48 hours
 Antiviral treatment may benefit patients hospitalized with influenza or bacterial
complications of influenza even if started after 48 hours of illness.
 Consider empiric antiviral treatment for patients with severe or progressive illness and
those with higher risk of complications

14. Oseltamivir
 Most widely used
neuraminidase inhibitor
 75 mg BD for 5 days, with
longer treatment for
critically ill patients.
 For chemoprophylaxis, the
dose is 75 mg once a day
for 1-2 weeks.
Peramivir
 IV neuraminidase
inhibitor for those unable
to tolerate oral
oseltamivir.
Baloxavir
 Approved for those 12 years and
older.
 Single PO dose
 40 mg for those 40-80 kg,
 80 mg for those > 80 kg.
 Not approved for
chemoprophylaxis.
Neuraminidase inhibitors

15. HERPES
SIMPLEX
VIRUS
INFECTIONS

16.  HSV-1 and HSV-2 are related double-
stranded DNA viruses that cause oral and
genital infections;
 Rarely, these result in devastating CNS
disease.

17. “Herpes simplex infections are treatable with antiviral drugs, making early
recognition of serious infection important”

18. Epidemiology of HSV
 HSV is common throughout the world.
 HSV-1 is usually acquired during childhood through nonsexual contact
 HSV-2 is almost always sexually transmitted
 Neonates with HSV infection have a high frequency of both visceral
involvement and CNS disease.
 Encephalitis in neonates is acquired from the maternal genital tract at the time
of delivery.

19.  HSV-1 typically resides in the trigeminal ganglia
 HSV-2 is found in the sacral ganglia.
 Reactivated virus travels to the cutaneous surface and results in localized
vesicular eruptions
 In herpes simplex encephalitis, virus gains access to the brain by the olfactory
or the trigeminal nerve, with a predilection for the medial and inferior temporal
lobes of the brain.

20.  Most healthy hosts are able to control the
virus and limit its replication to mucosal
surfaces.
 Multiorgan disease is much more common
in the immunosuppressed and in
neonates.

21.  Primary infections typically produce more extensive
lesions, often accompanied by systemic signs and
symptoms.
 Gingivostomatitis and pharyngitis are typical
manifestations of primary HSV-1 infection
 Recurrence presents as herpes labialis.
 Less common skin manifestations include herpetic
whitlow and herpes gladiatorum
Herpes gladiatorum

22. Eczema herpeticum
can occur in patients with atopic
dermatitis
Herpetic keratitis
presents as a painful, red eye
identified by characteristic dendritic
lesions on fluorescein slit lamp exam.

23.  HSV-1 and HSV-2 can cause identical
genital lesions.
 Genital HSV-2 is more common and has a
higher relapse rate,
 Primary genital infections can present with
aseptic meningitis, which is a complication
more common in women.

24.  The hallmark of HSV encephalitis is acute onset of fever and neurologic
symptoms.
 Patients can present with hemiparesis, cranial nerve abnormalities, ataxia, focal
seizures, and altered mental status or behavioral abnormalities.
 It can be difficult to distinguish HSV encephalitis from other types of
meningoencephalitis.

25.  Meningitis occurs in up to 25% of females with primary HSV-2 infections.
 HSV-2 meningitis, unlike encephalitis, has a benign course, and patients
recover uneventfully, although many patients have recurrent episodes.

26.  Organ transplant patients may develop esophagitis, hepatitis, colitis, and
pneumonia
 Severely burned patients are also prone to potentially fatal disease.
 HSV infections can also cause immune-mediated manifestations such as
erythema multiforme, hemolytic anemia, and thrombocytopenia.

27. Diagnosis of HSV
 Viral culture from the fluid of an unroofed vesicle
 PCR or a direct fluorescent antibody test have higher sensitivity.
 A Tzanck smear is not useful

28. HSV Encephalitis
Identification of temporal lobe lesions
on CT scan or MRI is strongly
suggestive of HSV encephalitis
An electroencephalogram shows
typical intermittent, high-amplitude
slow waves localized to the
temporal lobes.

29. CSF in HSV meningoencephalitis
 Lymphocytic pleocytosis with the presence of RBCs.
 Some have normal CSF parameters.
 PCR testing of CSF is the testing modality of choice for HSV meningoencephalitis
 Detectable viral DNA in CSF occurs within the first 24 hours, and results remain
positive for a week or longer.
 Multiplex PCR panels are available to test CSF for HSV and other viral,
bacterial, and fungal pathogens.

30.  IV acyclovir is the drug of choice in patients with HSV encephalitis or
disseminated disease and in immunocompromised patients with severe
mucocutaneous disease
 Even with early treatment, patients with HSV encephalitis have a high mortality.
 Without treatment, mortality is >70%.
 Survivors are often left with long-term neurologic sequelae.

31. Independent predictors of a poor outcome for patients with HSV encephalitis
 Glasgow Coma Scale score of ≤6
 Focal CNS lesions on CT scan
 Increased patient age
 Start of antiviral therapy >4 days after onset of symptoms.

32. Since it can be clinically difficult to distinguish meningitis from encephalitis,
consider adding acyclovir to empiric antibiotic therapy in patients with these
neurologic findings when the diagnosis of acute bacterial meningitis is also being
considered.

33.  Healthy patients with primary HSV-1 or HSV-2 infections can be treated with
oral acyclovir, valacyclovir, or famciclovir for 7 to 10 days.
 Recurrent herpes labialis usually does not require treatment.
 Those with severe or frequent recurrences may benefit from daily suppressive
therapy.

34. VARICELLA AND HERPES ZOSTER

35.  Higher incidence during winter and spring months.
 The infection rate: 60% to 100% in exposed individuals.
 Herpes zoster can occur once immune response against the virus wanes

36.  Vaccines are available to prevent both chickenpox and herpes zoster, although
neither is 100% effective.
 Varicella-zoster immune globulin - postexposure prophylaxis for nonimmune
pregnant women and the severely immunosuppressed.
 Healthy individuals who are not immune can be vaccinated after exposure.

37. SPREAD
 Droplet infection
 Direct contact with vesicle fluid in herpes zoster (low infectivity)
 Contagious until all the lesions have crusted over.
 VZV remains latent in the dorsal root ganglion and can later reactivate along
dermatomes, resulting in shingles

38. VARICELLA CLINICAL FEATURES
 Febrile illness with a vesicular rash.
 Nonspecific symptoms of headache,
malaise, and loss of appetite.

39.  The rash is superficial and appears in
crops
 Lesions at varying stages, including
papules, vesicles, and crusted lesions
 Lesions are concentrated more on the
torso and face and typically crust and
slough off after 1 to 2 weeks.

40. Complications
 more in extremes of age or the immunocompromised.
 Bacterial superinfections of skin lesions, most often with group A streptococci, can
cause serious illness including necrotizing fasciitis.
 Children with lymphoma and leukemia may develop progressive varicella in which
vesicles continue to erupt into the second week of illness, sometimes with visceral
involvement of the lung, liver, and brain.
 CNS complications such as cerebellar ataxia, meningitis, meningoencephalitis,
 vasculopathy.
 Pneumonitis can be severe and is more common in pregnant women

41. HERPES ZOSTER CLINICAL FEATURES
 Begins with a prodrome of malaise, headache, and
photophobia.
 Pain, itching, and paresthesias in one or more
dermatomes.
 Maculopapular rash that becomes vesicular.
 The eruption does not cross the midline
 Mostly affects the chest or face

42.  Herpes zoster oticus → The 7th cranial
nerve involvement → facial nerve
paralysis and lesions along the auditory
canal
 Herpes zoster ophthalmicus → corneal
damage →reactivation along the
ophthalmic distribution of the trigeminal
nerve

43. “Postherpetic neuralgia, pain that persists for >30 days”

44.  Herpes zoster involving more than three dermatomes is often a clue to an
immunodeficient condition.
 The presence of herpes zoster in a young, healthy person may be a sign of
HIV.
 In many cases of disseminated disease, the skin is the only involved structure.
 the virus may spread to the visceral organs and cause pneumonitis, hepatitis,
and encephalitis

45. DIAGNOSIS
 clinical diagnosis is sufficient in most cases
 Laboratory diagnosis aids in patients with atypical illness or severe disease.
● viral culture
● antigen testing
● polymerase chain reaction testing of vesicle fluid.

46.  chest radiograph if there are any breathing symptoms to assess for
pneumonitis. suspected neurologic involvement
● An MRI of the brain
● lumbar puncture
● PCR of CSF

47. VARICELLA TREATMENT
 Supportive Care For Chickenpox.
 Acyclovir And Similar Antiviral Agents Decrease The Number Of Lesions And
Shorten The Course Of Therapy If Started Within 24 Hours Of Rash Onset.
 Impact Of Treatment Is Modest, So It Is Not Routinely Recommended For
Those Who Are Otherwise Healthy.
 Secondary Skin Infections Are Typically Caused By Group A Streptococci And
Can Be Treated With A First-generation Cephalosporin.

48. Consider acyclovir for…..
 those at higher risk for complications
 patients with chronic skin or pulmonary disorders,
 those receiving long-term salicylate therapy
 immunocompromised patients.
 Varicella-zoster virus is less sensitive to antiviral medications than herpesvirus
and requires higher and more frequent dosing.

49. HERPES ZOSTER TREATMENT
Start antiviral medication within 72 hours of the onset of rash, and consider
treatment at >72 hours if new vesicles are still present or developing. Treat
immunocompromised patients regardless of the time since rash onset

50. Antiviral agents
 Hasten lesion resolution
 Reduce new lesions
 Reduce viral shedding
 Decrease acute pain
 Reduce the risk of severe disseminated disease in immunocompromised
……………….do not reduce the severity of postherpetic neuralgia.

51. Varicella vs Smallpox
The lesions of smallpox are larger and distributed more on the extremities, and all
lesions are at the same stage of development.

52. EPSTEIN-BARR VIRUS INFECTION

53. Causes
heterophile-positive infectious mononucleosis.
B-cell lymphoma
Hodgkin’s disease
Burkitt’s lymphoma
nasopharyngeal carcinoma.

54. CLINICAL FEATURES
 Infants and young children  asymptomatic/ mild pharyngitis.
 Teenagers and young adults  Symptomatic
 Fever, lymphadenopathy, and pharyngitis.
 Tonsillar exudates - often extensive and may be necrotic appearing
Splenomegaly in > 50%
 Symptoms resolve over 2 to 3 weeks
Severe fatigue is a prominent feature and can persist for months.

55. DIAGNOSIS
● Lymphocytosis with >50% lymphocytes
● Atypical lymphocytes on peripheral smear 
reactive cytotoxic T cells that can also be found in
CMV infection, HIV and viral hepatitis.

56. Monospot Test
 identifies heterophile antibodies that agglutinate animal erythrocytes
 The monospot test result may be negative early in the course of disease (first
days), requiring a second test later if unclear.
 The sensitivity of the test is also decreased in infants and the elderly.
 Testing is particularly important in pregnant patients, because some other
causes of heterophile-negative mononucleosis, such as toxoplasmosis and
cytomegalovirus, can be teratogenic.

57. Treatment
 Most cases are self-limited and not require specific therapy
 Rest and analgesia are the mainstays of therapy
 Corticosteroid use may increase complications and is recommended
only for patients with severe disease, such as upper airway obstruction,
neurologic disease, or hemolytic anemia.
 Acyclovir is active against Epstein-Barr virus, but is thought to be effective
only for oral hairy leukoplakia associated with human immunodeficiency virus
infection.
 Advise patients to avoid all contact sports for a minimum of 3 weeks
after illness onset to avoid splenic injury.

58. CYTOMEGALOVIRUS INFECTION

59. CMV
Transmissio
n

60.  Asymptomatic infections in most  life-threatening
pneumonia in transplant patients.
 It causes a primary infection and then recedes into lifelong
latency.
 Not highly contagious, and transmission requires repeated or
prolonged exposure
 teratogenic effects.

61. Clinical features
 Primary infection in healthy individuals is usually asymptomatic.
 Cytomegalovirus can cause a heterophile-negative infectious mononucleosis
syndrome
 prolonged fever,myalgias, and atypical lymphocytosis
 no exudative pharyngitis
 mild lymphadenopathy.
 Severe disease in the otherwise healthy host includes hepatitis, colitis,
Guillain-Barré syndrome, encephalitis, and hemolytic anemia.

62. Neonatal CMV
 Symptoms in infants can be devastating
○ Hepatosplenomegaly
○ Jaundice
○ Microcephaly
○ Petechiae
○ growth retardation.
 Severe infections carry a high mortality, and those who survive
often have neurologic sequelae

64. CMV in Immunocompromised
 Can be severe and involve any organ.
 Primary or the result of reactivation of latent virus.
 Infections after solid-organ and hematopoietic stem cell
transplantation are a leading cause of morbidity
 In HIV patients with CD4 counts <50 cells/mm3
○ retinitis is the most common manifestation, causing
painless loss of vision.
○ encephalopathy, colitis, and peripheral polyradiculopathy.

65. Diagnosis
 A specific diagnosis is usually not made in the ED.
 Body fluids such as urine, saliva, blood, tears, semen, and
vaginal fluid are antigen, polymerase chain reaction, and
antibody tested
 tissue is examined or cultured for diagnosis.
 The hallmark of CMV infection on histologic examination is a
large cell containing a large basophilic intranuclear “owl’s eye”
and intracytoplasmic inclusion bodies.

66. CMV Treatment
 ganciclovir, valganciclovir, foscarnet, and cidofovir.
 Illness in the otherwise healthy host is usually self-
limited and does not require antiviral therapy.
 Cytomegalovirus-induced infectious mononucleosis is
treated symptomatically.

67. MEASLES

68.  Measles = rubeola (Morbillivirus) / rubella (Rubivirus)
 Rubella infection is typically mild, but when contracted during pregnancy is
teratogenic.
 The current global measles epidemic is due to Rubeola.
 Rubeola is the most infectious virus known to humans and is communicable
before symptoms begin.

69.  Most measles deaths occur among children in developing countries, but
developed countries are now seeing outbreaks related to parents choosing not
to vaccinate their children, largely due to unfounded fears about vaccine safety.

70. Clinical features of Measles
 Incubation period of 10 to 14 days
 Illness starts with fever, malaise, cough, and runny nose
 often with conjunctivitis.
 Small, white Koplik’s spots appear on the buccal mucosa
early in the illness
 Followed by a red maculopapular rash that typically starts
on the head and spreads throughout the body.

71. Diagnosis
 Diagnosis is usually clinical, with pathognomonic Koplik’s spots and the
characteristic rash.
 Measles confirmation is by detecting immunoglobulin M antibodies, which are
present at rash onset.
 PCR testing of urine and throat specimens can distinguish true measles from
IgM elevation with recent vaccination.

72. Measles treatment
 Treatment is supportive
 ensuring adequate nutrition, especially vitamin A.
 Mortality
• in developed countries is <1 per 1000
• up to 20% to 30% among infants in developing countries, often from
pneumonia.
 Most measles suspects can be discharged home with instructions to watch for
symptoms of complications such as pneumonia or encephalitis.

73. ED
 EDs should have protocols for identification of measles suspects at initial point
of contact based on characteristic symptoms in the setting of local outbreak or
recent travel to an outbreak area.
 Measles suspects should be immediately placed in airborne isolation.
 Identify family contacts of high-risk suspects in the ED and offer vaccination.
 Save a log of potential exposures of both ED staff and other patients at the time
of the visit, in case it is later confirmed as measles

74. ARBOVIRAL INFECTIONS

75. Dengue fever
 Dengue virus is a common cause of fever and rash
in tropical areas with large mosquito populations
 Severe dengue hemorrhagic fever can develop in
locals who are exposed to a second infection with a
different serotype.
 A novel vaccine to all four serotypes is available in
many developing countries.

76. Chikungunya Fever
 causes rash, myalgias, arthralgias, and
fever.
 Although fatalities are rare, arthralgias can
be debilitating and last for months.

77. Yellow Fever
 Yellow fever is found in the tropics of Africa and
South America.
 The Aedes aegypti mosquito vector for the
yellow fever virus
 This mosquito can also spread dengue and
chikungunya viruses.

78. CLINICAL FEATURES
 Most arbovirus infections are either asymptomatic or cause a
nonspecific mild illness.
 Only a few individuals develop hemorrhagic fever or encephalitis.

79.  Severe human arboviral diseases most commonly manifest
1. fever and myalgia,
2. arthritis and rash,
3. Encephalitis
4. hemorrhagic fever.
Headache is a common symptom of most arboviral infections and may be quite
severe

80.  Hemorrhagic fever presents with bleeding from the gums, petechiae, and GI
tract.
 The classic presentation of viral encephalitis is fever, headache, and altered
level of consciousness.
 Patients can be lethargic and confused and occasionally present with seizures.
 In general, those at extremes of age are more likely to have severe
manifestations with these infections.

81. Diagnosis
 Obtaining a detailed travel and exposure history and knowing
local epidemiologic
 patterns help in diagnosing arboviral infections.
 Patients with encephalitis should undergo CT or MRI of the brain.
 MRI is more sensitive and may show foci of increased signal
intensity in the parenchyma.

82. CSF
 lymphocytic pleocytosis
 slightly elevated protein level,.
 When encephalitis is in the differential diagnosis, save an extra vial of
 cerebrospinal fluid for further testing, because less common infections
 are often diagnosed only with stepwise testing after more common
 causes have been ruled out.

83.  A presumptive diagnosis of the suspected arboviral infection can be made
based on an elevated immunoglobulin M level
 immunoglobulin M appears within a few days.
 Patients who are tested very early in the course of illness may have a
 false-negative result.
 Many arboviruses are antigenically similar and cross-react on testing.
 Arboviral infections are reportable to public health authorities in many areas.