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Microbiology MBBS > Bloodstream: Viral Hemorrhagic Fever, Malaria > Flashcards

Bloodstream: Viral Hemorrhagic Fever, Malaria Flashcards

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1
Q

Viral hemorrhagic fever are caused by

A
  1. Arboviruses: dengue, yellow fever viruses
  2. Filoviruses: Ebola, Marburg viruses
  3. Rodent borne viruses: Hantaviruses, arenaviruses
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2
Q

Common features of viral hemorrhagic fever

A

All are enveloped RNA viruses
Humans are not the natural reservoir
Symptoms: fatigue, 🤒, weakness, dizziness 😵‍💫, muscle aches
Only symptomatic treatment except for Lassa fever
No vaccine except for yellow fever and dengue

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3
Q

Arboviruses of India

A 
1. Hemorrhagic fever group:
 Dengue, KFD
2. Fever with arthralgia:
 Chikunguniya
3. Encephalitis:
Japanese encephalitis and West Nile encephalitis
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4
Q

Dengue

vector

A

Aedes aegypti (or A. albopictus)
Bite during day time
Nervous feeder (bites repeatedly to more than one person to complete a blood meal) ➡️ efficient vector
But A. albopictus is aggressive and concordant feeder.
Extrinsic incubation period of 8-10 days for infectivity, but then for life
Transovarial transmission

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5
Q

Dengue virus

basic pathogenesis

A
  1. 1° dengue infection:
    When a person is infected for the first time with any one serotype
  2. 2° dengue infection:
    Months to years later when the person is infected with a different serotype
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6
Q

Dengue

antibody response

A
  1. Neutralising: protective
    Against infective serotype: lifelong immunity
    Against others: diminishes over few months
  2. Non-neutralising: protects the serotype
    Heterotypic, i.e, produced serotypes except the infective one
    It inhibits bystander B cell activation - ADE antibody dependent enhancement
    ➡️ mononuclear cell recruitment and cytokines release
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7
Q

Dengue fever

according to traditional classification

A 
1. Abrupt onset of high 🤒:
 biphasic/break bone/ saddle back fever
2. Maculopapular rashes over chest and upper limbs 
3. Severe frontal headache
4. Muscle and joint pain
5. Lymphadenopathy
6. Retro-orbital pain
7. Loss of appetite, nausea, weakening
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8
Q

DHF Dengue hemorrhagic fever

A
  1. High grade continuous fever
  2. Hepatomegaly
  3. Thrombocytopenia
  4. Raised hematocrit by 20%
  5. Evidence of hemorrhages
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9
Q

Dengue shock syndrome

A

All the criteria of dengue hemorrhagic fever +

  1. Rapid and weak pulse
  2. Narrow pulse pressure
  3. Presence of cold and clammy skin
  4. Restlessness
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10
Q

2009 WHO classification of dengue

A
  1. Dengue with or without warning signs

2. Severe dengue

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11
Q

Dengue

factors determining the outcome

A
  1. Infecting serotype:
    Type 2 is apparently more dangerous
  2. Sequence of infection:
    Serotype 1 followed by serotype 2 can develop into DHF and DSS more often
  3. Age: Children less than 12 yr are more prone to develop DHF and DSS
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12
Q

Dengue during pregnancy

A

Perinatal transmission of dengue infection can occur
Newborn may present with fever, thrombocytopenia, ascites or pleural effusions
Typically on first week of life

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13
Q

Dengue

antigen detection

A

NS1 antigen detection
ELISA and ICT are used
Becomes detectable from day 1 of fever upto 18 days
Highly specific: differentiate b/w flaviviruses and also b/w different serotypes

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14
Q

Dengue

antibody levels in 1° infection

A

Antibody response is low and of low titre
IgM appears after 5 days of fever and disappears within 90 days
IgG is detectable at low titre in 14-21 days of illness and then slowly increases

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15
Q

Dengue

antibody levels in 2° infection

A

IgG rises rapidly:
• Often cross-reactive and may give false positive result after recent infection of vaccination with yellow fever or JE.
• Low levels remain detectable for over 60 years and is a useful indicator of past infection.
IgM is significantly low and may be undetectable

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16
Q

The recommended serological test for dengue in India

A

MAC-ELISA: Antibody capture ELISA
Double 🥪 ELISA detecting IgM, then serotype specific envelop protein antigen detection
(Signal enhancement by avidin-biotin complex ABC)
Limitation: Cross reactivity with other flaviviruses

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17
Q

Most specific but cumbersome serological tests for dengue

A

Plaque reduction test

Micro neutralisation test

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18
Q

Most specific test for dengue

A

Detection of specific genes of viral RNA (3’-UTR) by real time RT-PCR.
Most sensitive and specific
Detected in blood -1 to +5 days of onset of symptoms

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19
Q

Treatment of dengue

A 
No specific antiviral therapy
Symptomatic treatment like:
1. Replacement of plasma losses 
2. Correction of electrolyte and metabolic disturbances
3. Platelet transfusion if needed
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20
Q

Dengvaxia

A

CYD-TDV
Age: 9-45 years
Only in people previously infected with dengue
Not yet available in India

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21
Q

Chikungunya

virus and its transmission

A

Togaviridae family
Enveloped ss RNA viris
Spread via Aedes aegypti mainly
Rarely vertical transmission from mother to foetus or organ transplantation

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22
Q

Chikungunya

transmission cycle

A
  1. Urban cycle:
    b/w humans and Aedes aegypti which bites during daytime
  2. Sylvian/ jungle cycle:
    b/w 🐒 and forest species of Aedes
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23
Q

Chikungunya

acute clinical manifestations

A

Incubation: around 5 days
• 🤒 and severe joint pain worsened at morning
• Arthritis is polyarticular, migratory, edematous, mainly affecting small joints of wrist and ankles
• Other symptoms are headache, muscle pain, tenosynovitis or morbiliform skin rashes
• Chik sign out brownie nose appearance
Most patients recover within a week, except for joint pain

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24
Q

Chik disease or brownie nose appearance

A

Rarely seen in Chikungunya
Hyperpigmentation of centrofacial area
Due to 🔼 intraepidermal melanin retention triggered by Chikungunya

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25
Q

Chikungunya

high risk group

A
  1. Newborns
  2. Older adults >65 years
  3. Underlying hypertension, diabetes, or heart disease
    Only supportive treatment
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26
Q

Chikungunya

antibody changes

A

IgM appears after 4 days of infection and lasts for 3 months
IgG appears only after 2 weeks but lasts for years.
So detection of IgM or 4-fold rose in IgG is more important.

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27
Q

Chikungunya

recommended test

A

MAC-ELISA: IgM antibody capture
Good specificity and sensitivity
Only little cross-reactivity with other alphaviruses and dengue

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28
Q

Chikungunya

laboratory diagnostic measures

A
  1. MAC-ELISA
  2. Molecular method: rt-PCR for nsP1, naP4 genes
  3. Viral isolation
  4. Haematological findings like leukopenia with lymphocytes predominance, elevated ESR and C-reactive protein
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29
Q

Kyasanur forest disease KFD

A

Family flaviviridae
Enveloped ssRNA virus
Hard ticks (Hemaphysalis spinigera) are the vector
🐒 , rodents 🐀 and squirrels 🐿 are common hosts (🐒 are the amplifier hosts)
Reported in drier months

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30
Q

KFD

clinical manifestations

A

Incubation: 3-8 days
1. First stage: hemorrhagic 🤒
Acute high 🤒 with malaise and frontal headache, followed by hemorrhagic symptoms; bleeding from nasal cavity, throat, gums and GIT
2. Second stage: meningocephalitis 7-21 days after first stage

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31
Q

KFD

Laboratory diagnosis

A
  1. Virus isolation
  2. IgM antibody detection by ELISA
  3. nested RT-PCR and real time RT-PCR have been recently developed to detect viral RNA
  4. Leukopenia, thrombocytopenia, 🔽 hematocrit, albuminuria and abnormal CSF in 2nd stage
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32
Q

Filoviridae

A

Pleomorphic, mostly appears as long filamentous threads
Most fatal along the viral hemorrhagic fever
Eg., Ebola, Marburg viruses

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33
Q

Ebola virus

transmission

A
  1. Close contact with blood, sections, organs or other body fluids of infected animals like chimps, 🦍, fruit 🦇 or 🐒.
  2. Human-to-human transmission:
    Direct contact through broken skin or mucus membranes
    Body fluid, infected surfaces and materials
  3. HCW and family members/close contacts are at high risk
  4. Can stay in semen for 3 months, but sexual transmission unreported.
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34
Q

Ebola virus

clinical manifestations

A

Incubation: 2-12 days
🤒, headache, muscle pain and sore throat, followed by:
1. Abdominal pain, 🤮 and severe watery diarrhoea
2. Diffuse erythematous maculopapular rash, petechiae, ecchymosis/bruising; often leading to shock and death ☠️
Mortality: 25-90%

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35
Q

Ebola virus

antibody detection

A

ELISA detects both IgM and IgG separately by using recombinant nucleoprotein NP and glycoprotein GP antigens
IgM appears after 7 days of symptoms and lasts for 3-6 months
IgG appears after 14 days and lasts for 3-5 years
Other Ab detection assays include IFA and Ab-phage indicator assay

36
Q

Ebola virus
serum antigen test
electron microscopy 🔬

A

Detected by ELISA
The target proteins are: NP, VP40, GP
IHC staining and histopathology can also be used to localise viral Ag in tissue
e- 🔬: topical filamentous viruses can be seen

37
Q

Ebola virus

molecular methods

A

RT-PCR and real time RT-PCR assays are useful to detect specific RNA such as NP and GP gene 🧬.
Virus 🦠 can be detected 3 days after onset of 🤒 and remains positive for 2-3 weeks

38
Q

Ebola virus 🦠

Prevention

A
  1. Proper infection control and sterilisation (😷 and🧴)
  2. Isolation
  3. Avoid direct or indirect contact with blood, body fluids and secretions
  4. Avoid attending ⚰️ or wear PPE
  5. Monitoring for 21 days after returning from outbreak area
39
Q

Marburg virus 🦠

A

Viral hemorrhagic fever
Reported in Africa
Latest outbreak in Angola with 252 people affected and mortality rate of 90%

40
Q

Rodent borne viruses

A

Rodent borne viruses or roboviruses are transmitted from rodents to man by contact with infected body fluids or excretion.
They are maintained in nature by transmission from rodent to rodent and without participation of arthropod vectors.
Major rodent-borne viruses include: Hantaviruses and Arenaviruses

41
Q

Hantaviruses
Virus
Diagnosis

A

Family Bunyaviridae
Spherical, enveloped viruses containing triple segmented, negative ssRNA.
Diagnosis is by detection of viral RNA by RT-PCR

42
Q

Hantaviruses

Clinical manifestations

A
  1. Hemorrhagic fever with renal syndrome HFRS:
    But several members such as Hantaan 🦠, Dobrava 🦠, Puumala 🦠 and Seoul virus
  2. Hantaviruses pulmonary syndrome:
    By Sin Nombre virus
43
Q

Arenaviruses

A

Pleomorphic, 50-300 nm in size, enveloped with large, club shaped peplomers and contain a segmented ssRNA.
Grouped into: New world viruses and old world viruses

44
Q

Classification of Arenaviruses

A
  1. New world viruses:
    Include Junin, Machupa, Guanarito and Sabia viruses.
    They cause South American hemorrhagic fever
  2. Old world viruses:
    • Lassa viruses: hemorrhagic fever in Africa
    • Lymphocytic choriomeningitis LCM viruses: primarily infect 🐁, rarely causes meningitis in humans
45
Q

Malaria is caused by

A
  1. P. vivax
  2. P. falciparum
  3. P. ovale
    The above 3 are tertian - 48 hrs
  4. P. malariae: quartan - 72 hrs
  5. P. knowlesi - quotidian 24 hours
46
Q

Malaria

cases where sporozoite not the infective form

A

Trophozoite (or merozoite) is the infective form when it is rarely transmitted through blood transfusion or transplacentally

47
Q

Malaria

stages of pre-erythrocytic (hepatic) phase

A
  1. Sporozoites leave the circulation in 30 min
  2. Attachment to hepatocyte receptors and entry
  3. Trophozoite formation and feeding
  4. Schizogony: several nuclear divisions to form pre-erythrocytic schizont containing several merozoites
  5. Rupture of hepatocyte to release merozoites.
48
Q

Malaria

special points about pre-erythrocytic (hepatic) phase

A
  1. Circumsporozoite proteins involved in attachment to hepatocyte
  2. Negligible liver injury
  3. Lasts for 5-15 days
  4. Hypnozoites
49
Q

Hypnozoites

A

Some sporozoites of P. vivax and P. ovale do not develop further and may remain in liver as hypnozoites and may cause relapse after many years which should be differentiated from recrudescence

50
Q

Malaria

special points about erythrocytic phase

A
  1. Merozoites bind to glycophorin receptors on RBC, endocytosis and then in parasitophorous vacuole.
  2. Early trophozoites (ring form)
  3. Late trophozoite or amoeboid form
  4. Hemozoin formation
  5. Schizogony to form 6-30 erythrocytic schizont
  6. RBC rupture ➡️ malarial paroxysm
51
Q

Malaria

early and late trophozoite

A
  1. Early trophozoite or ring form:
    Annular or signet ring in appearance containing a central vacuole with a peripheral thin rim of cytoplasms and nucleus
    It enlarges and becomes more irregular to form
  2. Late trophozoite or amoeboid form:
    It undergoes schizogony to produce 6-30 daughter merozoites (erythrocytic schizont) arranged as rosette which can invade other RBCs
52
Q

Why in P. falciparum only ring forms are seen in peripheral blood examination

A

In P. falciparum, the later stages of erythrocytic cycle occur in capillaries of brain and internal organs.

53
Q

Malaria

gametocytes

A

Some merozoites transform into round microgametocyte and macrogametocyte (except falciparum where it is 🌙 or 🍌 shaped)
They are capable of transmission only when they are mature, viable and present in sufficient density.

54
Q

Malaria

mosquito 🦟 cycle

A
  1. Microgametocyte undergoes exflagellation and divided into 8 flagellated actively motile bodies called male gametes
    Macro gametocyte directly develops into one macrogamete.
  2. Zygote
  3. Ookinette: motile elongated formed in midgut
  4. Oocyst
  5. Sporozoite formation by meiosis
  6. Release and migration to salivary gland
    This in total extends 1-4 weeks (extrinsic incubation period)
55
Q

Oocyst, ookinette and sporozoites of malaria in 🦟

A

Ookinette: motile elongated formed in midgut
Oocyst: ookinette penetrates stomach wall becomes rounded and covered by a thin elastic membrane to form oocyst
Sporozoites: 4 spindle shaped sporozoites produced by meiosis
They are released and then they migrate to salivary gland’s

56
Q

Benign malaria

A 
Milder in nature
Can be caused by all 4 species
Characterised by triad of:
1. Febrile paroxysm 
2. Anaemia
3. Splenomegaly due to macrophage proliferation to ingest RBCs
57
Q

Stages of malarial febrile paroxysm

A
  1. Cold stage:
    Lasts for 15 minutes to 1 hr
    The patient feels lassitude, headache, nausea 🤢 , intense cold 🥶, chills and rigor
  2. Hot stage:
    Patient develops a high grade 🤒 of 39-41°C and dry burning skin
    Head ache persists but 🤢🔽
  3. Sweating stage:
    🤒🔽 with profuse sweating 😓
    Skin becomes cold and moist, patient feels relieved 😌 and often 💤
    Lasts for 2-4 hours
58
Q

Deviations from benign malarial febrile paroxysm

A
  1. In P. falciparum, the 🤒 is more irregular or even continuous with marked prostration, headache and 🤢
  2. The classical paroxysm may not be always present due to maturation of generations of parasites at different times.
59
Q

Causes of anemia in benign malarial fever

A
  1. Parasite induced RBC destruction
  2. Splenic removal of both infected RBC and uninfected RBC coated with immune complexes
  3. Bone 🦴 marrow suppression
60
Q

Sequestration of P. falciparum

A

In deep visceral organs like 🧠, kidney,… by
Cytoadherence: binding of infected RBCs to endothelial cells by its antigen called P. f erythrocyte membrane protein PfEMP-1.
This leads to blockade of vessels, congestion and hypoxia of internal organs.
Also they avoid frequent spleen passage
PfEMP-1 undergoes frequent antigenic variation.

61
Q

Complications of falciparum malaria

A
  1. Cerebral malaria: most serious
  2. Pernicious malaria:
    Black water malaria + algid malaria + septicemic malaria
  3. Pulmonary edema and ARDS
  4. Hypoglycemia: 👶, 🤰, poor prognosis, following quinine Rx
  5. Renal failure
  6. Bleeding w/o DIC
  7. Severe jaundice: in adults
  8. Severe normochromic, normocytic anemia
  9. Acidosis
62
Q

Black water anemia

A

Sudden intravascular hemolysis followed by fever, hemoglobinuria, and dark urine
1. Occurs following quinine treatment to previously infected falciparum patients
2. Ab develop against parasitised and quininised RBC.
Later immunocomplex formation followed by complement mediated massive destruction of parasitised and normal RBCs.

63
Q

Algid malaria

Septicemic malaria

A

Algid malaria: cold clammy skin, hypotension, peripheral circulatory failure and profound shock.
Septicemic malaria: high-grade 🤒 with dissemination of parasite to various organs leading to multiorgan failure.

64
Q

Chronic complications of malaria

A
  1. Tropical splenomegaly syndrome/ hyper active malarial splenomegaly
  2. Quartan malarial nephropathy:
    immunocomplex deposition in glomeruli by P. malariae
  3. Promotes Burkitt’s lymphoma:
    Due to immunosuppression.
65
Q

Tropical splenomegaly syndrome

Hyperactive malarial splenomegaly

A

Due to abnormal immunologic response to repeated malaria infections and characterised by 🔼 IgM.
Patients respond well to anti-malarial chemoprophylaxis

66
Q

Special features of transfusion malaria (which includes needle stick injury, organ transplantation)

A
  1. The infective form can be intra-erythrocytic forms but not gametocytes.
  2. There is no pre-erythrocytic stage and no relapse ➡️
  3. Radical chemotherapy with primaquine is unnecessary.
  4. Incubation period is often short
67
Q

Malaria in pregnancy

A

It increases risk of fetal distress syndrome and can result in premature labor, low birth weight and still birth.
In areas of high malarial transmission, 🤰 are particularly susceptible to severe anemia, hypoglycemia and acute pulmonary edema.

68
Q

Innate immunity of malaria depends on:

A 
1. Age of RBC:
 vivax and ovale attacks young RBC
 malariae attacks older RBC
2. Nature of hemoglobin ✖️ falciparum 
3. Hereditary ovalocytosis are resistant
4. G6PD deficiency
5. Duffy negative RBC 
 Duffy blood group acts as receipts for P. vivax
6. Age: children are more prone but not infants
7. Nutritional status: paradoxically
69
Q

Malaria

acquired immunity

A 
1. Humoral immunity:
 Against both asexual and sexual forms
2. Cell mediated immunity
3. Premunition/ incomplete:
 Immunity against Plasmodium remains till original infection is active
70
Q

Transmission of malaria is proportional to:

A
  1. Density of vector and no. of human bites per day per 🦟
  2. Time of 🦟 bite, more after dusk
  3. 🦟 longevity for sexual development of plasmodium
  4. Optimal temperature, humidity (60%) and rainfall
71
Q

Malaria

microscopic tests

A
  1. Peripheral blood smear: gold standard
    • thick smear: more sensitive
    • thin smear: speciation can be done
  2. Fluorescence microscopy - Kawamoto’s technique
    Nuclear DNA stained green
  3. Quantitative buffs coat examination:
    Parasitised RBCs appear as brilliant green dots.
72
Q

Malaria

speciation using thin smear - species wise

A
  1. vivax: amoeboid ring form and schizont
  2. falciparum: ring forms (multiple ring, accole and headphone shaped ring forms), 🍌 shaped gametocytes
  3. malariae: band forms
  4. ovale: enlarged fimbriated oval RBC with ring forms
73
Q

Malaria

Peripheral blood smear - specimen

A

Site:
• great toe in infants
•👂 or finger prick in the rest
Capillary blood is taken few hours after height of paroxysm before anti malaria drugs
Smeared and stained by Romanowsky stain within 1hr
Examined twice to confirm absence

74
Q

Malaria

features involved in speciation

A
  1. RBC size
  2. Pigments: prop. to severity
    Dark brown except vivax (yellowish-brown)
  3. Schizont
  4. Gametocytes:
    🍌 shaped in falciparum
  5. Ring forms
75
Q

Malaria

RBC size vs species

A

Normal: falciparum, malariae
Enlarged: vivax
Enlarged and fimbriated margin: ovale

76
Q

Malaria

speciation based on schizont

A

P. vivax: large, which completely fills the enlarged RBC
contains 12-24 merozoites/schizont.
P. malariae and P. ovale: small, fills 3/4th or bit more
contains 8 merozoites/schizont.
P. falciparum: schizonts are not seen

77
Q

Malaria

ring forms and speciation

A

Ring forms are most important in speciation.
P. vivax:
• Rings are 2.5 μm, occupies 1/3rd
• late trophozoites are amoeboid shape
P. falciparum:
• rings are 1.5 μm, occupies 1/6th, maybe multiple/cell
• Accole form: ring attached to RBC membrane
• double-dot/headphone shaped ring form: nucleus fragmented
P. malariae:
• early trophozoites are similar to vivax
• late trophozoite is band shaped
P. ovale:
• similar to vivax, but in ovale shaped RBC

78
Q

Malaria
rapid diagnostic tests RDTs detecting antigens
the antigens are:

A 
Produced by all Plasmodium species:
1. Parasite lactate dehydrogenase pLDH
2. Parasite aldolase
Produced by only P. falciparum:
3. Histidine rich protein-2: HRP-II
79
Q

Malaria

Advantages of RDTs rapid diagnostic tests detecting antigens

A
  1. Sensitivity: at >100 parasites/μL they are sensitive, but not so much otherwise
  2. Prognosis: though not better than🔬
  3. Pregnancy: HRP-II is reliable marker to diagnose it in🤰
  4. Severity: intensity of band
80
Q

Malaria

disadvantages of RDTs rapid diagnostic tests detecting antigens

A
  1. Speciation of non-falciparum species impossible
  2. Expensive than 🔬
  3. Gametocytes not detected
  4. Low sensitivity
  5. Not developed for knowlesi
81
Q

Severe malaria treatment

A 
DoC include:
1. IV artemisinin derivatives:
 Against sexual RBC stages and gametocytes
2. IV quinine:
 Against non-falciparum gametocytes
82
Q

Anti-malarial drugs

A 
1. Quinolines:
 Chloroquine, quinine, mefloquine, primaquine
2. Artemisinin and its derivatives
3. Atovaquone
4. Proguanil
5. Pyrimethamine
6. Sulfadiazine and sulfadoxine
7. Tetracycline and doxycycline
83
Q

Factors contributing to emergence of anti malarial drug resistance
Treatment

A
  1. Longer half life of drug
  2. Mutation in parasite gene 🧬
  3. Inadequate and irregular usage of drug
  4. Host immunity
    Rx: combination of drugs like ACT artemisinin combination therapy
84
Q

Mechanisms of drug resistant malaria

A
  1. Chloroquine resistance:
    Mutation in 🧬 encoding for transport proteins like PfCRT (chlq rs transporter) and PfMDR1 (multi drug rs 🧬 1)
  2. Antifolate resistance: pyrimethamine
    mutation of DHFR dihydrofolate reductase
85
Q

Chemoprophylaxis for malaria

A

Is recommended for: travelers 🧳, migrant laborers, military 🪖 personnel.
Types:
1. Short term - doxycycline
2. Long term - mefloquine

86
Q

Vector control strategies

A 
Anti adult measures:
1. Residual spraying
2. Space application
3. Individual protection
Anti larval measures:
1. Larvicide
2. Source reduction
3. Biological larvicide
87
Q

Problems of making a malarial vaccine

A
  1. The vaccine 💉 candidates are poor inducer of CMI
  2. Antigenic variation in malarial antigens such as PfEMP
  3. Different immune mechanisms occur in different stages of malaria life cycle

Microbiology MBBS (16 decks)

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