Micro - Evals 6 Flashcards
VIRUSES AFFECTING CVS AND LYMPHATICS
Paramyxovirus Arbovirus Flavivirus - Dengue, Yellow Fever Alphavirus - Chikungunya Togavirus - Rubella virus Picornavirus - Poliovirus and Coxsackievirus Herpesvirus - CMV and EBV Filovirus
Type of viremia that is responsible for viral spread of Paramyxovirus to the salivary glands, testes, ovaries, pancreas and CNS
Primary viremia
Type of viremia that is responsible for generalized viral spread of Paramyxovirus to the salivary glands and other glands, as well as the other body sites including the kidneys
Secondary viremia
Incubation period of Paramyxovirus
2-4 weeks
Primary characteristic of mumps infection
Gopher-like swelling of the cheeks
Prognosis of mumps
Self-limiting
Anti-pyretics can be given
Site of primary replication of mumps virus
Nasal or URT
Complications of mumps
Orchitis and epididymitis
Pancreatitis
Viral meningitis
Hearing loss
Most important in diagnosing mumps
History and PE
Samples used for serologic testing for mumps
Saliva - present after 1 week since onset
Urine - present upto 2 weeks since onset
CSF
Timing of collection of sample
Within a few days of onset of disease
Prevention of mumps
Live attenuated mumps vaccine
Virus families under Arboviruses
Bunyaviridae
Flaviviridae
Togaviridae
Diseases caused by Arboviruses
Mild undifferentiated fevers
Severe encephalitis
Life-threatening hemorrhagic fever
Virus responsible for Crimean-Congo hemorrhagic fever
Nairovirus
Most important vectors of Arboviruses
Mosquitoes
Ticks
Flies
Gnats
Incubation period of Arboviruses
1 week
Characteristics of morbiliform rash
Maculopapular
Secondary to endothelial cell damage and increased vascular permeability
Flaviviruses are sensitive to
Heat
UV radiation
Disinfectants
Glycoproteins in Flavivirus lipid envelope
M and E glycoproteins
E glycoprotein biologic properties
Viral cellularity attachment
Endosomal membrane function
Display of sites mediating hemaglutination and viral neutralization
Most prevalent flavivirus infection and biggest Arbovirus problem in the world
Dengue
Transmission of dengue
Man-arthropod-man
Also vertical transmission, passively acquired antibodies, pre-existing heterologous dengue antibody
Principal mosquito vector of Dengue and Chikungunya
Aedes aegypti (polka-dotted day-biters)
Syndrome produced by heterologous immunity to dengue
Dengue-Hemorrhagic Fever or Dengue Shock Syndrome
Site of viral replication of Flavivirus
Monocytes
Increased vascular permeability in DHF-DSS may be due to
Increased levels of soluble TNF
IFN-gamma
Complement system activation
Dengue type 1: ?
Dengue type 2: ?
Dengue type 1: Dengue fever
Dengue type 2: Dengue hemorrhagic fever
Cause of immunopathologic response if DHF
Virus-antibody complex
Characteristic symptoms of Breakbone fever
Myalgia and deep bone pain
Saddleback form fever
Scarlatiniform rash
Severe frontal headache and retro-orbital pain (adults)
Differentiating feature of DHF from Dengue fever
It has defervescence within 2-7 days
Characteristic features of DSS
Shock and hemoconcentration
Laboratory diagnosing test with high sensitivity and high specificity
Rapid immunochromatographic test
Contraindicated drug when treating Dengue
Aspirin to prevent Reye’s syndrome and hemostatic problems
Prevention of Dengue
Mosquito eradication (4 o'clock habit) No effective vaccine
Transmission of Yellow Fever (2 cycles)
Urban yellow fever
Jungle yellow fever
Human-to-human transmission by A. aegypti
Urban yellow fever
Infected monkeys-to-humans transmission by Haemagogus
Jungle yellow fever
Clinical presentation of frank yellow fever
Sever hemorrhagic manifestations
Oliguria
Hypotension
Diagnosis of yellow fever
Usually clinical
If available: viral isolation, postmortem, serology
Prevention of yellow fever
Live attenuated vaccine
Three major groups of Alphavirus
West African
Central African
Asian
Common physical symptoms of Chikungunya
Redness of eyes
Difficulty looking at light
Prevention of Chikungunya
Piricardin containing insect repellants
Treating clothes with permethrin
Host of Togavirus
Humans only
No invertebrate host
Togavirus transmission
Aerosol droplets
Drug that inhibits Togavirus
Amantadine
Immunity from Togavirus
Life long immunity but reinfections can still occur
Clinical features of Rubella
Maculopapular rash
Lymphadenopathy
Fever
Athropathy
Risk of Rubella during pregnancy
Precoception: minimal
0-12 weeks: 100% risk; spontaneous abortion
13-16 weeks: deafness and retinopathy
After 16 weeks: normal development
Classical triad of Congenital Rubella Syndrome
Cataracts
Heart defects
Sensorineural deafness
Prevention of CRS
Terminate pregnancy
Diagnosis of Rubella
Serial rising titers of antibody - HAI, EIA
Placental biopsy and specific IgM fetal blood
Falling rubella antibody titer indicates
Passively acquired maternal antibody
Rising rubella antibody titer indicates
Rubella infection
Rubella IgM in newborn infant serum
Transplacental infection
Prevention of Rubella infection
Antenatal screening
Live attenuated vaccine - women should not get prenant at least 3 months after vaccination
Non-enveloped Picornavirus that causes acute enteroviral infection of the spinal cord that may cause neuromuscular paralysis but are mostly subclinical
Poliovirus
Poliovirus serotypes that cause severe disease
Serotypes 1 and 3
Only reservoir of Poliovirus
Humans, most commonly children
Poliovirus transmission
Fecal-oral route
Flies as mechanical vectors
Incubation period of Poliovirus
1-2 weeks
Antibodies occur in
Large intestine and tonsils
Serum
Confers life long immunity
Polio must be differentiation of these diseases in order to be diagnosed
GBS
Infant botulism
Encephalomyelitis
Prevention
Salk vaccine
Sabin vaccine
Inactivated polio vaccine
Salk vaccine
Oral polio vaccine
Sabin vaccine
Coxsackievirus commonly causes
Transient neonatal infection
Coxsackievirus transmission
Fecal contamination
Incubation period of coxsackievirus
2-9 days
Diseases caused by CoxA virus
Herpangina
Acute hemorrhagic conjunctivitis
Aseptic meningitis
Hand-foot-and-mouth disease
Diseases caused by CoxB virus
Pleurodynia
Aseptic meningitis
Severe generalized disease of infants
Myocarditis and pericarditis
Mainstay in diagnosing Coxsackievirus
Viral isolation
Herpesvirus transmitted via intimate contact
Cytomegalovirus
Common symptoms of CMV
Hepatomegaly, spenomegaly, jaundice, capillary bleeding, microcephaly, ocular inflammation
Disease caused by CMV
CMV Mononucleosis Disseminated CMV CMV pneumonitis Perinatal CMV Congenital CMV infection Cytomegalic Inclusion DIsease
Most common congenital viral infection
Second most common cause of mental handicap
Congenital CMV infection
Treatment of CMV
Gancyclovir
Foscarnet
Hyperimmune CMV Ig
Principal mode of transmission of EBV
Direct oral contact
Contamination with saliva
Also fomites and arthropods
Diseases caused by EBV
Infectious Mononucleosis/Kissing Disease Burkitt's lymphoma Nasopharyngeal carcinoma EBV induced lymphoproliferative diseases EBV associated lymphomas
Notable sign of Infectious Mononucleosis
Sudden leukocytosis
Constant feature of Nasopharyngeal carcinoma
High antibody titers to EBV
Drug that reduces EBV shedding from the nasopharynx
Acyclovir
Filovirus that caused 2014 West African outbreak
Zaire Ebola virus
Suspected transmission of Filovirus
Fruit bats Human-to-human via direct contact Healthcare workers Mourners of infected cadavers Sexually Breastfeeding
Incubation period for Filovirus
2-21 days
PARASITES AFFECTING CVS AND LYMPHATICS
Plasmodium Wuchereria Brugia Trypanosoma Leishmania Schistosoma Babesiosis
Most common protozoan disease affecting man
Plasmodium - Malaria
Malarial paroxysm
Cyclic fever
Chills
Sweating
Mode of transmission of Plasmodium
Vector-borne - pregnant female Anopheles
Needle-sharing
TRUE or FALSE.
Malaria is not a major problem in the Philippines.
True
Host of Plasmodium
Humans and mosquitoes
Infective stage of Plasmodium to man
Sporozoites
Schizont development occurs during this stage
Liver stage
Entry point of Plasmodium into the liver
Sentinel Kupffer cell
Most common victims of Malaria
Pregnant women
Children
Main mode of transmission of Plasmodium
Natural transmission
Mode of transmission without sporozoites, exo-erythrocytic cycle or liver phase and hypnozoites
Induces transmission
Vectors in Malarial transmission
Anopheles flavirostris Anopheles litoralis Anopheles maculatus Anopheles balbancensis Anopheles mangyanus
Primary malarial vector in the Philippines
Anopheles flavirostris
Malarial vector commonly found in brackish water in Palawan
Anopheles litoralis
Parts of proboscis
2 pairs of cutting stylets
1 pain of hollow tubes
Contents of mosquito’s saliva
Anti-hemostatic enzymes
Anti-inflammatory subtance
RoleS of mosquitoes in Malaria
Definitive host
Biological vector
Role of man in Malaria
Intermediate host
Parasite ligand and host receptor for entry of sporozoites into liver cells
Parasite ligand: CSP
Host receptor: Unknown
Parasite ligand and host receptor for entry of merozoites into RBC (P. falciparum)
Parasite ligand: EBA175
Host receptor: Glycophorin A
Parasite ligand and host receptor for entry of merozoites into RBC (P. vivax)
Parasite ligand: Pv153
Host receptor: Duffy factor
Parasite ligand and host receptor for cytoadherence of P. falciparum-infected RBC to endothelium
Parasite ligand: PfEMP-1 Host receptor: CD36 (endothelium and platelets) Parasite ligand: KAHRP Host receptor: ICAM-1 (brain) Parasite ligand: PfEMP-2 Host receptor: CSA (placenta)
3 patholophysiologic changes in Malaria
RBC lysis
Knob formation of infected RBC
Metabolic effect (hypoglycemia and acidosis)
Histopathologic changes in organs affected
Vascular congestion
Edema
Malarial pigment (HEMOZOIN) deposition
Cytokines involved in the pathogenesis of malaria
TNF
IL-1b, IL-6, IL-8
Interferon-y
NO
Effects of cytokines in low concentrations
Protective
Inhibit growth of parasites
Hemostatic agent
Clinical features of Malaria
Malarial proxysms Jaundice Pallor and dizziness Changes in sensorium Tachycardia Dry and pale lips Enlarged spleen and liver
Malarial paroxysm that is usually mild without complications seen in P. vivax and P. ovale, every 48 hours
Benign Tertian
Malarial paroxysm that is usually severe with complications seen in P. falciparum, every 48 hours
Malignant Tertian
Malarial paroxysm that is periodical every 72 hours seen in P. malariae
Quartan
Malarial paroxysm that is periodical every 24 hours seen in P. falciparum and P. knowlesi
Quotidian
Induces fever in Malaria
Hemozoin either directly from RBC lysis or indirectly through GPI
Cause of anemia in Malaria
Maturing schizonts either from direct RBC lysis or increased utilization of hemoglobin
Factors that lead to hypoglycemia in Malaria
Limited food intake
Increase glucose consumption
Increase Quinin-induces insulin resistance
Inhibition of gluconeogenesis
Result of hypoglycemia in Malaria
Compensatory glycogenolysis
Laboratory features of Malaria
Decreased Hgb and Hct
Ring-like parasite in blood smear
Small infected RBC
Mature RBC
Due to P. falciparum, P. malariae, P. knowlesi
Large infected RBC
Younger RBC
Due to P. falciparum P. vivax, P. ovale
Diagnostic test of choice of Plasmodium species identification
Thin smear
Number of chromatin dots in trophozoite and schizont
Trophozoite = 1-2 chromatin dots Schizont = 2-4 chromatin dots
Amoeboid and compact form
Schuffner’s dots
Fine stippling
P. vivax
Band form
James or Ziemann’s dots
Regular daisy-like apperance of merozoites
P. malariae
Number of merozoites
P. falciparum = maximum of 32 meroizoites
P. vivax = maximum 24 merozoites
P. ovale and P. malariae = maximum of 12 merozoites
Maurer’s cleft/dots
Acole forms
Multiple parasitism
Banana-shaped gametocyte, may have Laveran’s bibs
P. falciparum
Amoeboid and compact form
Schuffner’s dots
Fine stippling
Irregular rosette-like clusters of merozoites
P. ovale
Band form
No stippling
Multiple parasitism
P. knowlesi
Deadliest and causes most severe form of malaria
P. falciparum
Causes recrudescence
P. falciparum and P. malariae
Laboratory test that detects histidine-rich proteins 2 in a strip of filter paper
ParaSight F
Causes relapse
P. vivax and P. ovale
Causes reinfection
All types
End stage of Lymphatic filariasis
Elephantiasis
Agents that cause filariasis
W. bancrofti
B. malayi
B. timori
Transmission of filarial worms
Oviviparous female mosquito bites
Clinical feature
Unrecognized recurrent lymphedema
Diagnostic stage of filariasis
Microfilariae/L1
Infective stage to humans
L3
Role of mosquitoes
Intermediate host
Biological vector
Common filarial vectors
W. bancrofti: Anopheles, Aedes, Culex
B. malayi: Anopheles, Mansonia
Day biting mosquito
Aedes
Night biting mosquitoes
Culex and Mansonia
Causes occult filariasis
B. malayi
Causes scrotal enlargement and lymphedema or elephantiasis
W. bancrofti
TRUE or FALSE.
Presence of worms can elicit both humoral and cell-mediated
True
Most common change occuring at the lymphatics
Polypoid endolymphangitis
Effect of dead or dying adult worms in the tissues
Fibrinoid necrosis Filarial granuloma (Meyers-Kouvenaar bodies)
Pathognomonic feature of filariasis seen as a pronounced eosinophilic infiltration in nodular patterns around the worm
Filarial granuloma (Meyers-Kouvenaar bodies)
Clinical form of lymphatic filariasis with microfilarimia
Asymptomatic
Acute
Chronic
Clinical form of lymphatic filariasis without microfilarimia
Occult
Patient has hidden damage to the lymphatic system and kidneys
Asymptomatic
Patient has attacks of filarial fever increasing with severity, pain and inflammation of lymph nodes and ducts, nausea and vomiting
Acute
Elephantiasis, hydrocele in males, enlarged breast in females
Chronic
Hypersensitivity reaction to the worm
Occult
Most common manifestation of lymphatic filariasis
Asymptomatic
Manifestation of occult filariasis
Pulmonary tropical eosinophilia syndrome
Clinical presentation of Pulmonary Tropical Eosinophil syndrome
Pulmonary symptoms
Radiologic changes
Nonspecific weight loss
Increase IgE, eosinoohilia and increased antimalarial AB
Conditions that lead to elephantiasis
Chronic edema in subcutaneous tissue
Proliferation of fibrous CT
Thickening of epidermis
Diagnosis of filariasis
Identification of microfilariae in blood smear by microscopic examination
Methods of microfilariae detection
Wet smear
Thick blood film
Blood concentration techniques
Morphology of W. bancrofti during microscopy
With hyaline sheath Short cephalic space Regular with graceful curve Round, larger, well-separated body nuclei No nuclei, pointed tip
Morphology of B. malayi during microscopy
With hyaline sheath Long cephalic space Irregular with kinking curves Small, overlapping body nuclei Two widely spaced nuclei, blunted tip
Imaging technique characterized by dancing worms
Ultrasonography
Imaging technique that use radioloactive opaque dye
Lymphangiography
Imaging technique that use radiolabeled albumin
Lymphoscintigraphy
Gold standard biochemical test in diagnosing filariasis
ELISA
Drug of choice for filariasis
Diethylcarbamazine
Alternative treatment for filariasis if the patient has eye involvement
Ivermectin
Preventive mass drug administration
Albendazole with Diethylcarbamazine
Albendazole with Ivermectin
Developmental stage of blood flagellates seen in tissue samples
Amastigote
Developmental stage of blood flagellates seen in blood samples
Trypomastigote
Causative agent of African sleeping sickness
T. brucei
Life cycle/Development of Trypanosoma spp.
Heteroxenous
Asexual reproduction of Trypanosoma
Binary fission
Evading mechanism of T. brucei
Antigenic variation
Distinctive features of T. brucei
Changes from slender trypanosome into a stumpy form
VSG switching which allows second wave of parasitemia
Characteristics of T. b. gambiense
Gambian trypanosomiasis, W. African sleeping sickness Humans are primary reservoir Winterbottom sign Chronic/late CNS manifestation Low parasitemia Meingo-encephalitism Lymph fluid is best microscopy specimen
Characteristics of T. b. rhodesiense
Rhodesian trypanosimiasis, E. African sleeping sickness
Animals are primary reservoir
More fatal and aggressive
High parasitemia
CNS involvement glomerulonephritis or myocarditis
Infective stage of Trypanosoma spp.
Metacyclic trypomastigote
Diagnostic stage of Trypanosoma spp.
Trypomastigotes
Stage of African sleeping sickness characterized by the presence of Trypanosomal chancre and Winterbottom sign
Stage 1 Hemolymphatic