Why Would I Need One? If your doctor orders this test, it’s because they think you might have a systemic infection and they want to check for certain kinds of germs in your blood. It can help them come up with the best treatment for you. Written by WebMD Editorial Contributors Medically Reviewed by Carol DerSarkissian, MD on December 08, 2022 A blood culture test helps your doctor figure out if you have a kind of infection that is in your bloodstream and can affect your entire body. Doctors call this a systemic infection. The test checks a sample of your blood for bacteria or yeast that might be causing the infection. Your doctor might order the test if you have symptoms that may include: Fever or chills Fatigue Peeing less often than normal Nausea Confusion Faster heart rate or breathing If your infection is more severe, you might have: Inflammation in different areas of your body Small blood clots forming in your small blood vessels A serious drop in your blood pressure Organ failure Mouthwash sampling Patients were asked to rinse and gargle 10 cc of normal saline (0.9%) for about 10–20 s and then spit the fluid into a sterile container. In addition, other solutions were tested with a small number of patients, in order to compare it to the standard saline solution, which included the following: is wet blood film? o A wet blood film is used for the detection of. living trypanosomes, microfilariae of filarial. worms etc Procedure for blood wet mount First, wear the groves. Take a clean and grease-free slide. Add one drop of blood and then also add a drop of New methylene blue ( supravital stain). Mix it properly and apply a coverslip over a uniform suspension without creating bubbles. Examine the entire 22- by 22-mm coverslip systematically with the low power objective (10X ) and low light intensity. If any suspicious objects encounter, examine with the high dry objective (40X) as shown above image and below video. Procedure for blood wet mount First, wear the groves. Take a clean and grease-free slide. Add one drop of blood and then also add a drop of New methylene blue ( supravital stain). Mix it properly and apply a coverslip over a uniform suspension without creating bubbles. Using lens paper, gently wipe two glass slides to remove any dust or glass fragments. ... Mix blood thoroughly (if not a fresh sample). ... Using your dominant hand, place the edge of the other slide at an approximately 35-45⁰ angle on the first glass slide, in front of the blood drop One cycle consists of-one ECV whole blood collection in kit bowl, centrifugation of bowl to separate components, collection of required component (platelets) in collection bag and finally return other constituents like red cells, leucocytes and plasma to donor. This cycle is repeated till therapeutic dose is attained

1. ‫اليمنية‬‫ية‬‫ر‬‫الجمهو‬
‫الحديدة‬‫جامعة‬
‫الصحية‬‫والعلوم‬‫الطب‬‫كلية‬
‫البشري‬‫الطب‬‫قسم‬
‫الثالث‬ ‫المستوى‬
:

‫فـــــارس‬ ‫خالــــــد‬
.

‫الشريـــف‬ ‫محمـــد‬
.

‫جمــاح‬ ‫عبدالمجيد‬
.

‫الوصابـــــي‬ ‫هـمام‬
.

‫الموسمــــي‬ ‫حسن‬
.

‫بــــــــــاذيب‬ ‫منــى‬
.

‫الضحـــــوي‬ ‫نـوار‬
.

‫المزجاجـــي‬ ‫أيـات‬
.

‫الكلعــــــي‬ ‫رويــدا‬
.

‫طـــــــــارق‬ ‫نهــى‬
.

2. Mumps

3. Mumps
Mumps Is An Acute, Non suppurative ,Self-limited,
Systemic Viral Illness Characterized By The Swelling Of
One Or More Of The Salivary Glands, Typically The Parotid
Glands.
Epidemiology
1_Incidence: Drastically Declined In The US Since The Introduction Of
The MMR Vaccine.
2_Peak Age: 5–14 Years Of Age
3_Sex: ♂ = ♀ For Parotitis (However, Males Are Three Times More
Likely To Have CNS Complications)
4_Mumps occurs endemically worldwide.
5_Cases appear throughout the year in hot climates and peak in the winter
and spring in temperate climates.

4. Etiology
Pathogen: Mumps virus from the Paramyxoviridae family
Transmission:
Humans are the only host and the virus is transmitted
via airborne droplets.
Direct contact with contaminated saliva or respiratory
secretions
Sharing cups .
Infectivity:
Highly infectious
Affected individuals are contagious in asymptomatic
case , symptomatic case , and 7 days after disappear
swelling .

5. Virology
Non segmented , -ssRNA , linear genome that is 15,384
neucleotides in length .
Helical symmetry .
Has envelope " lipid membrane " , roughly spherical shapes .
Virion vary in size from 100 -600 nm in diameter .
The virus contains (seven major) structural proteins:
1_nucleocapsid-associated protein (NP).
2_phosphoprotein (P)
3_polymerase protein (L) are associated with the nucleocapsid.
4_membrane or matrix (M) protein.
5_two glycoproteins, a hemagglutinin-neuraminidase (HN).
6_fusion (F) molecule.
7_ small hydrophobic (SH) .
The virus genes have been sequenced and the gene order for
mumps virus is (3-NP–P–M–F–SH–HN–L-5).

6. Pathophysiology
Nasopharyngeal entry → replication of the virus in the mucous
membranes and lymph nodes → viremia and secondary infection
of the salivary glands (particularly the parotid gland) → further
dissemination possible (lacrimal, thyroid, and mammary
glands, pancreas, testes, ovaries, CNS)

7. Clinical features
Incubation period: 16–18 days [6]
Prodrome
 Duration: 3–4 days
 Symptoms: low-grade fever , malaise, headache
Classic course: inflammation of the salivary glands, particularly parotitis [5][7]
Duration of parotitis: at least 2 days (may persist > 10 days)
Symptoms
 May initially present with local tenderness, pain, and earache
 Unilateral swelling of the salivary gland (lateral cheek and jaw area); During the course of
disease, both salivary glands are usually swollen.
 Redness in the area of the parotid duct
 Possible protruding ears
 Loss of appetite.
 Muscle aches.
 Headache.
Chronic courses are rare.
Subclinical presentation [6]
Nonspecific or predominantly respiratory symptoms &
Asymptomatic (in 15–20% of cases).

8. Complications
Orchitis is inflammationof the testis
Epidemiology: most common complication of mumps in
postpubertal male individuals (20–30% in
unvaccinated postpubertal and 6–7% in vaccinated males) [6][8]
 Clinical features
 Sudden onset of fever, nausea, vomiting
 Swollen and tender affected testicle(s); primarily unilateral, although
bilateral in ∼ 15% of cases
 Complications: may lead to atrophy and, in rare
cases, hypofertility
 Other complications
 Oophoritis inflammation of an overy in 5-10% of post-pubertal
women.
 eididymitis about 85% of the time, typically occurring before
orchitis.
 Aseptic meningitis (1–10% of cases): predominantly mild
course and usually no permanent sequelae

9. Encephalitis (< 1% of cases)
 Reduced consciousness, seizures
 Neurological deficits: cranial nerve palsy, hemiplegia, sensorineural
hearing loss (rare)
Acute pancreatitis (< 1% of cases)
 Vomiting, nausea, upper abdominal pain
 ↑ Lipase in addition to ↑ amylase
 Diabetes mellitus type I (delayed complication) [6]
Hearing loss (extremely rare)
Meningoencephalitis inflammation of the brain and its
surrounding membranes.
Nephritis inflammation of the kidneys, which is rare because
kidney involvement in mumps is usually benign but leads
to presence of the virus in urine

16. Diagnostics
Laboratory tests, if available, should be conducted to confirm the
suspected cases (especially if presentation is atypical or there is a
mumps outbreak).
 Pathogen detection
 Real-time reverse transcriptase PCR (rRT-PCR) on
serum or buccal or oral swab
 Viral culture (e.g., on CSF, urine, or saliva)
 Serology: Positive serum IgM suggests recent infection and
confirms the diagnosis.
Positive serum IgG in absence of IgM indicate past infection
 Relative lymphocytosis
 ↑ CRP, ↑ ESR
 ↑ Amylase

18.  Differential diagnoses

19. Treatment
Mumps is usually self-limited with a good prognosis
(unless complications arise). Treatment is mainly
supportive care.
 Medication for pain and fever (e.g.,
acetaminophen).
 Bedrest.
 Adequate fluid intake.
 Avoidance of acidic foods and drinks.
 Ice packs to soothe parotitis.

20. Prevention
General measurements [4]
 Isolate infected patients (up to 5 days after onset of symptoms).
 Mass vaccination of susceptible people
 Mumps is a reportable disease and all cases should be reported to the
local health departments.
Primary immunization: a live attenuated vaccine in
combination with measles and rubella vaccine (i.e., ) and, if
necessary, varicella (MMRV) MMR
 Via two doses: first dose at 12–15 months, second dose at 4–6
years (See “Immunization schedule.”) [9]
 Because of maternal antibodies and thereby a weakened immune
response, early vaccination should be avoided.
Mumps vaccination during the first trimester in pregnancy may
lead to embryonal death.

21. Measles

22. Introduction
Measles is a childhood infection caused by a virus. It is also
called rubeola. It spreads easily and can be serious and
even fatal for small children.

23. Epidemiology
• Distribution: Measles typically occurs in regions with
low vaccination rates and in resource-
limited countries.
• Peak incidence: < 12 months of age.
• Infectivity :
o ∼ 90 %
o Highly contagious 4 days before and up to 4 days after the
onset of exanthem stage.
Etiology
• Pathogen:
Measles virus (MV), a member of the Morbillivirus
genus belonging to the Paramyxoviridae family.
• Route of transmission:
direct contact with or inhalation of virus-
containing droplets.

24. Virology
• The measles virus genome is non-segmented, negative-
sense single-stranded RNA.
• The RNA genome is enclosed in a lipid-containing
envelope derived from the host cell.
• The sequence 3′-N,P,V,C,M,F,H,L-5′ encodes eight viral
proteins, two of which (V and C) are nonstructural
proteins.
• Of the six structural proteins, large protein (L), and
nucleoprotein (N) form the helical nucleocapsid housing
the viral RNA.
• The hemagglutinin protein (H), fusion protein (F), and
matrix protein (M), together with lipids from the host cell
membrane, form the viral envelope.
• The phosphoprotein (p) acts as RNA polymerase
cofactor.

25. • The hemagglutinin (H) protein is responsible for
attachment to the cellular receptors, and the fusion (f)
protein mediates the fusion of the virus and host
membrane.
• Measles virus grow in human amnion cells and the
amniotic cavity of chick embryo.

26. Clinical features
Four stage of infection
STAGE 1 ( INCUBATION ) :
Incubation period ∼ 6–21 days (13 days )
A symptomatic
STAGE 2 ( PRODROMAL )
occur for 2-4 day
Fever , malaise
3Cs conjunctivitis, coryza , cough.

27. STAGE 3 ( EXANTHEM )
Koplik spots :
• Occur prior to exanthem
• White , gray , blue spots on erythematous base
Maculopapular rash :
• Occur 2-4 days after fever
• Macule : flat skin lesion less than 1 cm in diameter
• Papule : raised skin lesion less than 1 cm in diameter

28. Lymphadenopathy.
Pharyngitis.
Splenomegaly .
Diarrhea .
STAGE 4 ( RECOVERY )
The cough may persist for another week and may be the
last remaining symptom.

29. Complications:
1. Subacute sclerosing panencephalitis (SSPE)
• Definition :It is a lethal, generalized, demyelinating
inflammation of the brain caused by
persistent measles virus infection.
• Epidemiology : Primarily affects males between 8 and
11 years of age.
• Usually develops ≥ 7 years after measles infection.
• Symptoms :
• Characterized by four clinical stages:
Stage I: dementia, personality changes.
Stage II: epilepsy, myoclonus, autonomic dysfunction
Stage III: decerebration, spasticity, extrapyramidal
symptoms.
Stage IV: vegetative state, autonomic failure.

30. 2. Bacterial superinfection.
o Otitis media
o Pneumonia (most common cause of death)
o Laryngotracheitis
3. Gastroenteritis.
4. Meningitis.
5. Acute encephalitis.
o Frequency: ∼ 1:1000
o Develops within days of infection
o Acute disseminated encephalomyelitis may
develop within weeks.
6. Giant cell pneumonia (viral, most commonly seen
in immunosuppressed individuals).

31. Prognosis
• The prognosis of measles infection is good in
uncomplicated cases.
• Fatal courses are more likely
in newborns and immunocompromised patients.
• High fatality rate in resource-limited countries due
to secondary bacterial infections.
Diagnostics
Measles should be suspected in a patient with
typical clinical findings. Laboratory tests are
always necessary to confirm the diagnosis.
• CBC: ↓ leukocytes, ↓ platelets
• Serology:
Gold standard: detection of Measles-specific
IgM antibodies
IgG antibodies

32. • Identification of pathogen:
direct virus detection via reverse-
transcriptase polymerase chain reaction (RT-PCR)
possible
• Biopsy:
affected lymph nodes show
paracortical hyperplasia and Warthin-Finkeldey
cells (multinucleated giant cells formed
by lymphocytic fusion).
Treatment
• Symptomatic treatment.
• Vitamin A supplementation reduces morbidity and
mortality (especially in malnourished children).
• PEP in patients without prior vaccination.

33. Prevention (Immunization)
 Primary immunization
Indications:
• Every infant.
• Adults born after 1957 with unknown immunization or incomplete
status.
Method:
• Live vaccination with attenuated virus in combination with
mumps and rubella (MMR) vaccine and possibly varicella
(MMRV) vaccine
• Infants: two vaccinations during childhood
 Postexposure prophylaxis (PEP)
Indication: negative or indeterminate serology
Methods:
• Active immunization for immunocompetent individuals after
direct exposure.
• Passive immunization for chronically ill and
immunocompromised individuals.
Further measures for contact persons: avoidance of communal
facilities.

34. Rubella

35. Rubella
Rubella is a single-stranded RNA virus, which is the only
member of the genus Rubivirus within the family Togaviridae.
The outer envelope protein E1 is the viral haemagglutinin
protein responsible for binding to the cell receptors to initiate
infection.
Epidemiology
1-A rare disease in the US following the implementation of the
MMR vaccine.
2-Rubella has a worldwide prevalence.
3-Before the introduction of vaccination, it circulated in
epidemic form with an epidemic cycle every 6–8 years.

36. Etiology
Pathogen
o Rubella virus, an RNA virus of the family Matonaviridae
o Prior to 2019, the rubella virus was classified as the sole
member of the Rubivirus genus in the Togaviridae family.
o Humans are the only hosts.
Route of transmission
o Respiratory droplets or transplacental.
o Infectivity: 7 days prior to and 7 days following the
appearance of an exanthema.
o Low infectivity and virulence.
Taxonomy
Domain = Viruses
Group = Group IV ((+) ssRNA)
Family = Togaviridae
Genus = Rubivirus
Species = Rubella Virus

37. virology
Enveloped, spherical, 70-80nm in diameter. The capsid is
not icosahedric and bound to the membrane . Envelope
glycoproteins are assembled in helical organization.
Genome

38. Clinical features
Patients with rubella infection are asymptomatic in ∼ 50% of
cases. Young children have a far milder course than older
children and adults; the latter group often presents with
prodromal symptoms, other systemic complaints (e.g., arthritis),
and a longer duration of infection.
Prodromal phase
Incubation period: 2–3 weeks after infection
Duration: 1–5 days
Findings
o Post-auricular and suboccipital lymphadenopathy and
occasionally splenomegaly.
o Mild and nonspecific symptoms such as low-grade fever, mild
sore throat, conjunctivitis, headache, and aching joints.
o Forchheimer sign: enanthem of the soft palates.

39. Exanthema phase
Duration: lasts 2–3 days.
Findings
o Fine, nonconfluent, pink maculopapular rash.
#Begins at the head, primarily behind the ears, extends to
the trunk and extremities, sparing palms and soles.
#Rash may be itchy in adults
o Polyarthritis.
Complications
Chronic arthritis (especially women)
Thrombocytopenic purpura
Rubella during pregnancy (TORCH infection): congenital
rubella syndrome.
Rare: rubella encephalitis, bronchitis, otitis, myocarditis,
pericarditis.

40. Prognosis
The disease usually has a benign course and the exanthem
disappears rapidly. Joint pain may persist for several weeks;
arthralgia may persist up to a month in adults.
Diagnostics
Although rubella infection may be considered a clinical
diagnosis, laboratory confirmation is necessary for certain
patient groups to assess the risk of complications such as e.g.,
congenital rubella in pregnant women or encephalitis.
Laboratory tests [2][3] o CBC: leukocytopenia with relative
lymphocytosis and increased plasma cells o Confirmatory test:
serology Detection of IgM antibodies. ≥ 4-fold increase in
IgG titer.
For prenatal and congenital diagnosis → see congenital
rubella syndrome.

41. Differential diagnoses

42. Treatment
No treatment will shorten the course of rubella infection, and symptoms
don't usually need to be treated because they're often mild. However,
doctors often recommend isolation from others — especially pregnant
women — during the infectious period.
Prevention (Immunization)
Live attenuated virus that is administered in combination with the
measles and mumps vaccine (see immunization schedule).
Two vaccinations are recommended because of potential non-
responders (5%):
o First dose: 12–15 months of age.
o Second dose: 4–6 years of age or at least 28 days
following the first dose.
Check vaccination status
o ELISA (preferred method), latex agglutination,
hemagglutination inhibition, or immunofluorescent antibody
assay.
o A titer of ≥ 1:32 indicates immunity to rubella.

43. Women of child-bearing age, without vaccination or unclear
vaccine status, should be vaccinated prior to pregnancy!
Precautions during infection
Patients with rubella infection should be isolated for 7 days
after the onset of the rash.
Precautions regarding droplet transmission should be
taken.
Reporting regulations
Rubella cases need to be reported to the CDC or to the
National Center for Immunization and Respiratory Diseases
(NCIRD) within 24 hours of confirmation.

44. Congenital rubella infection
Epidemiology
Most mothers have been vaccinated, so congenital infection is
very rare.
Pathogen
Rubella virus Transmission
Mother
o Mainly via airborne droplets
o See “Rubella.”.
Fetus
o Transplacental from infected mother
o Risk of fetal infection is high in the first trimester, decreased
in the second trimester and then increased again in the third
trimester.
o Risk of congenital rubella syndrome .
1–12 weeks gestation (period of organogenesis): highest risk.
12–20 weeks gestation: very low.
> 20 weeks gestation: no documented cases.

45. Clinical features
Intrauterine rubella infection: miscarriage, preterm birth, fetal
growth restriction (especially likely if infection occurs during the
first trimester).
Congenital rubella syndrome.
o Triad of congenital rubella syndrome.
Cardiac defect: most common defect (e.g., patent ductus
arteriosus, pulmonary artery stenosis).
Cataracts: Other eye manifestations may also occur later in
life, including glaucoma and salt and pepper retinopathy
(abnormal retinal pigmentation).
Cochlear defect: bilateral sensorineural hearing loss.
o Early features.
Hepatosplenomegaly, jaundice.
Hemolytic anemia, thrombocytopenia.
Petechiae and purpura, i.e., blueberry muffin rash (due to extramedullary
hematopoiesis in the skin).
Transient meningitis and/or encephalitis.
Pneumonia

46. o Late features.
CNS defects: microcephaly, intellectual disability,
panencephalitis.
Skeletal abnormalities.
Endocrine disorders (e.g., diabetes, thyroid
dysfunction).
Vascular disease.
Immune defects

47. Diagnosis
Newborn and mother.
o PCR for rubella RNA (throat swab, CSF).
o Serology (abnormally high or persistent concentrations of IgM and/or
IgG antibodies) o Viral culture (nasopharynx, blood).
Fetus
o IgM antibody serology (chorionic villi, amniotic fluid).
o PCR for rubella RNA (chorionic villi, amniotic fluid).
Treatment
Intrauterine rubella infection.
o < 16 weeks: Counsel about potential maternal-fetal transmission and
the possibility of terminating the pregnancy.
o > 16 weeks: reassurance and symptomatic therapy (e.g.,
acetaminophen)
Congenital rubella syndrome: supportive care (based on individual
disease manifestations) and surveillance (including monitoring for late-
term complications).

48. Prevention
Immunization of seronegative women before pregnancy.
Nationally notifiable condition: Suspected congenital
rubella syndrome must be reported to the local or state
health department.