INFECTIOUS DISEASE REVIEW

General introduction
Q1. 3 basic conditions that constitute the epidemic process of an infectious disease?
Ans. an external agent, a susceptible host, and an environment

Q2. What are the diagnostic criteria for ID?

Ans. Isolation of the Agent in Culture, Detection of a Specific Host Immune Response of the
Infectious
Agent in Tissue Sections, and Discovery of the Etiologic Agents of Emerging Infectious Diseases.
Lab tests
( blood, urine), throat swabs, stool samples, lumbar puncture.

Q3. What are the key to control and eradicate ID?

a. Geographic and Environmental Controls
b. Potential Reservoirs
A microbe and associated disease can not be eradicated if the microbe can persist and multiply in a
reservoir.
c. Transmissibility
The inherent rate of a microbe's ability to cause secondary infections is defined by an organism's
reproductive rate in a fully susceptible (R0) and partially susceptible (R) population.
d. Natural Resistance to Reinfection
Eradication depends on reducing susceptible populations in potentially endemic areas, long-lived
protection through immunization or natural disease is important to successful programs.
e. Laboratory Containment.00
Laboratory specimens containing the organism targeted for eradication could serve as reservoirs.
f. Disease Surveillance
Surveillance and response systems need to be more efficient than the targeted agent's transmission
rate.
g. Interventions
Interventions may be designed for environmental control of microbes, isolation (quarantine) of
clinically
infectious individuals to limit their contact with susceptible persons, treatment of clinical cases to
limit the
duration of infectiousness, or reduction in the infected pool of individuals through
immunoprophylaxis or
chemoprophylaxis.

Q4. What is the difference between latent infection and carrier stage?
Ans. The difference between latent infection and carrier stage is as noted, a carrier is a person with
inapparent infection who is capable of transmitting the pathogen to others. Asymptomatic or passive
or
healthy carriers are those who never experience symptoms despite being infected but a person who is
in
the latent stage will experience symptoms in the near future as it is the pre-infection period. Both are
capable of transmitting the pathogen but only the person in the latent infection stage is at the risk of
experiencing symptoms later on.

Epidemic hemorrhage fever

1.clinical staging
5 progressive stages: Febrile Phase →Hypotensive Phase → Oliguric Phase →Diuretic Phase
→Convalescent Phase
Ferile stage
• Fever : 39-40,3-7 days
• Toxic symptoms :
Pain - Headache,lumbago,orbital pain
Gastrointestinal symptoms: nausea,vomiting,abdominal pain and diarrhea
• Capillary damage signs
Hyperemia: Flush over face, neck and chest skin
Hemorrhage : petechia, ecchymosis, or stripe-shaped bleeding in chest and back
skin,conjunctiva bleeding. For a partial cases, hematuria, DIC
Exudative edema: mainly babular conjunctiva edema. palpebra edema and face edema
• Kidney damage signs
Proteinuria, sometimes with casts, blood cells and membrane-shaped substance consisting
of protein, blood cells and mucosal epithelia.

Hypotensive Phase
Lasts for hours or days
• Blood pressure decrease, hypovolemia, shock (primary shock)
• Worsening of bleeding manifestations: petechiae, epistaxis, gastrointestinal and intracranial bleeding
• Levels of urea and creatinine in blood rise, proteinuria, leukocytosis, thrombocytopenia.
• atypical lymphocytes >10%

33% of all HFRS deaths are linked to multi-organ hypoperfusion at this stage

Oliguric Phase
 Lasts 3-7 days
Oliguria: urine output <400 ml /d
Anuria: urine out put<50 ml/d
 Hemorrhagic symptoms continue:
Epistaxis,conjunctival hemorrhage,cerebral hemorrhage, gastrointestinal bleeding and
extensive purpura.
 Onset of renal failure
Symptoms associated with uremia
Water-sodium retention: Hypentension; pulmonary edema; ascites
Acidosis, fluid and electrolyte imbalance, BUN↑ ，Cr ↑
 Severe complications: cardiac failure ,pulmonary edema, and cerebral bleeding.
o 54 50% of fatalities during this phase

Diuretic Phase
• Lasts a few days to a few weeks.
• Characterized by diuresis and hyposthenuria
• migratory stage :400-2000ml/d, although the urine output increases, blood urea and
creatinine still rise.
• earlier polyuric stage :more than 2000ml/d, azotemia does not improve, the symptoms still
are severe.
• later polyuric stage: more than 3000ml/d, the urine output increases per day, the azotemia
improve.
• Clinical recovery begins
• Urine output : 3-6 liters / day.
• Dehydration, electrolyte imbalance, or infection will occur.

Fluid replacement is inadequate→ secondary shock

Convalescent Phase
• Urine return to 1000-2000ml/24h
• Normal appetite
• Taking 1-3 months for recovering

Five phase be not seen in every case.hypotension and /or oliguria phase may be absent
in atypical cases.
Unusual complication, such as neurologic sequela, hypopituitarism or chronic renal failure was rarely
experienced

2.trean ment principle of each clincal stage of

Treatment in febrile phase
• Bed rest , strict maintenance of fluid balance
• Observe blood pressure,record the urine output
• Ribavirin has shown to be effective during the first 5 days of the HFRS illness.
To relieve the permeability of blood vessle:
Rutosids and vitamin C 80
• Management of the fever and toxic symptoms
Physical cooling
Antipyretic can be used carefully.
Short course dexamethasone

Treatment in hypotensive phase

Principle of treatment:
► Supplement blood volume
► Correct acidosis
1>.Supplement blood volume
A.Principle: early rapidly adequate
B:kinds of fluids:Crystalloid fluids and Colloid fluids containing suitable glucose, electrolytes and
vitamins:
• Ringer’s Solution
• Normal saline solution
• Dextran, albumin
• Plasma,, Artificial plasma
2>Correct metabolic acidosis
5% sodium bicarbonate solution.
3>.Blood vessel activating drugs
for hypotension and shock:dopamine, norepinephrine ,654-2

Treatment in oliguric phase

• Maintenance of internal environment homeostasis
Restrict the volume of infusion
Daily urine volume + 500-700ml
Control the azotemia
Supply sufficient carbohydrate to reduce the protein degradation
Maintaining electrolyte balance : Treatment of Hyperkalemia
Correction of acidosis : 5% Sodium Bicarbonate Injection

Diuretics: furosemide
Consider Dialysis in following conditions:
• Severe azotemia
• Fluid overload that cannot be managed with diuretics
• Hyperkalemia refractory to medical therapy
• Severe acid-base disturbances

Dialysis therapy
for serious azotemia
 ▲very important, save life
▲Hemodialysis or Peritoneal dialysis
Marker of giving Dialysis therapy:
Oliguria lasts for 4 days or anuria lasts
for 24 hours with one of following five signs:
• a>.Seral BUN >28.56mmol/L;
• b>.BUN increasing more than 7.14mmol/L
• every day;
• c>.Blood potassium > 6mmol/L;
• d>.hypervolemia or/and pulmonary edema;
• e>.being terrible fretful or cerebral edema.

Diuretic phase
• Adequate replacement of fluid and electrolytes
• Prevent secondary infection : Antibiotics with nephrotoxic potential should be avoided

Convalescent phase
• intensive nutrition and have a good rest.
• Examination renal function, blood pressure, pituitary function at regular interval

1.The main reason for early shock in HFRS is

A. Infection.
B. Blood plasma-losing
C. Hypervolemia
D. Hemorrhage
E. Vomiting .

2. The patient had fever, lumbago, headache for three days. Physical examination: drunken face,
petechiae in axillary folds, chemosis. Blood routine test: WBC 19×109 /L，N 83%, PLT
20×109 /L. Urine protein (+++), RBC 3-5/HP .The diagnosis may be
A.Typhoid fever
B.Typhus
C.Acute glumerulonephritis
D.Epidemic hemorrhagic fever

3. Typical hemorrhagic fever with renal syndrome caused by Hantaan virus evolve in
five identifiable stages:______, ______, ______, ______ and ______.
4. Give a introduction about the management principle of the oliguric phase of the
hemorrhagic fever with renal syndrome
5. Male, 30 years old, farmer. he was admitted because of fever , headache and lumbar pain for 4 days
.he was in good health in the past. PE: T 39℃, BP110/70mmHg, flushing on the face, conjunctival
congestion, petechiae are observed in the axillary folds. Both of lung were clear,
and the heart rate was normal. The abdomen was flat and soft , the liver and the spleen couldn’t be
palpable, lightly percussion pain in renal region, shifting dullness negative.

Laboratory findings:
Blood routine:WBC:15×109/L,PLT:70×109/L
Urine routine:protein＋,BUN:20mmol/L.CR:433umol/L.

• 1.What is the most possible diagnosis do you

think? and what is the proof of diagnosis?
• 2.What do you do to make diagnosis clear?
• Laboratory findings:
Progressive Thrombocytopenia, left-shifted leukocytosis, presence of abnormal lymphocyte ,abnormal
renal function, positive urine protein ,detect HFRS-Ab and so on.(elisa,rt-pcr)

AIDS
1.tramsnission route
Sexual contact : Vaginal,Anal,Oral(Heterosexual; Homosexual)
Blood or blood products : Blood transfusions, Sharing needles(IDU; tattoos or body piercing),
Occupational exposure(health care wokers being infected through accidents with needle sticks)
Vertical transmission : mother to child(The major cause of HIV infection in children)
• Pregnancy
• Labor
• Delivery
• Breast feeding

2.HIV damage which cells

Major target cells
• CD4+ T lymphocytes
• Monoctyes/macrophages
Minor target cells
• Langerhan’s cells
• CD34+ monoctye precursors
• triple negative(CD3/CD4/CD8) thymocytes,
• dendritic cells

3.how long I ncubation period

The period from infection to development of anti-HIV antibodies is usually less than 1 month but may
be up to 3 months

4.common tumor of AIDS

Kaposi sarcoma
Lymphoma(nonhodgkin)

5.CINICAL manifestation of AIDS

(1) constitutional symptoms: Fever, malaise, anorexia, diarrhea, loss of body weight etc. also known
as AIDS related complex (ARC).
(2) Central nervous system symptoms: Headache, epilepsy, progressive dementia, paraplegia etc.
(3) Severe opportunistic infections: Pneumocystic Carinii
Pneumonia (PCP), Cryptococcal meningitis, pulmonary tuberculosis, Candidiasis, oral hairy
leucoplakia, cryptosporidiosis, Histoplasmosis etc.
(4) Opportunistic malignancies: Kaposi sarcoma, non-Hodgkin lymphoma etc.
(5) Other disorders associated with severe immune suppression:Chronic lymphoid interstitial
pneumonitis etc.

Malaria
1.1 laboratory examination to diagnose malaria
 Giemsa-stained thick and thin blood smears – 95% sensitive( Gold standard for laboratory
confirmation of malaria.)
 Fluorescent microscopy – 90% sensitive, 70% specific
 PCR – nearly 100% sensitive and specific, but expensive
 Antigen detection from serum – fast, useful in field

1.2 clinical manifestation

 – Fever
– Chills
– Sweats
– Headaches
– Nausea and vomiting
– Body aches
– General malaise

1.3 drugs to prevent recurrence and relapse

• Artemisinines
• Chloroquine
• Mefloquine
• Piperaquine
• Aminoquinolines
Effect on gametocyte and bradysporozoite
• Primaquine
• Tafenoquine

1.4 what causes malaria to relapse?

Relapses occur because P. vivax have dormant liver stage parasites (hypnozoites) that may reactivate.

1.5 How to diagnose malaria: epidemic clinical and lab diagnosis

• Epidemiology history
a) Pandemic area
b) Bitten by mosquito
c) Blood infusion
• Clinical symptoms:
– Fever
– Chills
– Sweats
– Headaches
– Nausea and
vomiting
– Body aches
– General malaise
• Physical examinations
– Elevated temperature
– Perspiration
– Weakness
– Enlarged spleen.
• Lab findings
 Giemsa-stained thick and thin blood smears – 95% sensitive
 Fluorescent microscopy – 90% sensitive, 70% specific
 PCR – nearly 100% sensitive and specific, but expensive
 Antigen detection from serum – fast, useful in field

Cholera
1.clinical stages
A)Stage of diarrhea and vomiting
1. Diarrhea : – Abrupt onset
– Watery diarrhea
– Without obvious abdominal Pain
– Without fever, strain or tenesmus
 – “rice-water” stool
 cloudy, white, watery, without smell
 containing flecks of mucus
 no blood and fecal odor
 similar to water in which rice has been washed
2. Vomitting – Following the beginning of diarrhea
– Without nausea
– Vomitus is a clear and alkaline watery fluid

B) Dehydration Stage
a) Irritability
b) sleepless
c) anxiety
d) dysphoric
e) coma
f) irregular heartbeat（Arrhythmia）
g) Extra dry skin or mucus
h) Sunken Eyes
i) Lethargy
j) Abdominal pain
k) Irritable bowel syndrome IBS
l) Muscle cramps
m) electrolyte imbalance

C) Convalescent Stage
Dehydration has been corrected
• Pulse
• Breathe
• Mental status
• The urine
• The skin

2.pathogenesis of cholera
 3. fecal characterectics of cholera
Rice water stool
4. most important treatment of cholera
A) Replacing the fluids and electrolytes
1)ORS
Oral Rehydration Solution
2)Intravenous fluids
Severe infection
unable to drink
persistent vomitin
B)Antmicrobial treatment : Ciprofloxacin, norfloxacin, sulfamethoxazole complex,
doxycycline

Dengue
Common serotypes: There are four serotypes of dengue virus (DEN-1, DEN-2, DEN-3 and DEN-4).

Main transmission rotes

•People get dengue fever after the bite of an infected Aedesmosquito.
•Mosquitoes become infected when they bite infected humans, and later transmit infection to other
people they bite.

Lab tests
1. Detection of dengue virus genomic sequences in serum or cerebrospinal fluid samples by
polymerase chain reaction PCR).
2. The detection of NS1 to make an early diagnosis of dengue virus infection.
3. Dengue-specific IgM and IgG ELISA are widely used, as it is relatively inexpensive.
4. A fourfold rise or greater in antibody titer is diagnostic.
5. IgMIgG ratio:
> 1:2 - primary dengue infection
< 1:2 - secondary dengue infection
Typical febrile type of fever
typical febrile pattern in dengue fever is known as "biphasic fever." It consists of an initial acute
febrile phase followed by a defervescence phase.

Viral hepatitis
Transmissionroute of hepatitis A
2. Routes of Transmission
fecal oral (Hepatitis A, E)
blood, body fluids (Hepatitis B, C)
vertical transmission
(mother to newborn, perinatal transmission)
Sexual contact

Cause of acute hepatitis A bleeding : degeneration and necrosis. Portal hypertension can cause blood
to be redirected to smaller veins.
Strained by the extra pressure, these smaller veins can burst, causing serious bleeding.

Hepatitis b virus replicantion markers

Pregenomic RNA (pgRNA) serves as a template for HBV replication and its presence in cells is used
as a marker for viral replication. HepB-DNA

Diagnose differential acute vs acute severe hepatitis

1) Acute: onset quickly.
- General symptoms: fever, fatigue, discomfort.
- Symptoms of the digestive tract: vomiting, nausea. jaundice.
- ALT elevated
- Hepatitis A develops quickly.
- B and C are relatively slow.
2) Chronic. Longer than 6 months mild moderate severe
3) Severe Fulminant shorter than 14 days
Subacute longer than 14 days
Chronic on chronic hepatitis or cirrhosis bases.

Scrub thypus
definition
Acute febrile infectious disease
Caused by Rickettsia tsutsugamushi
Transmitted by the bite of chiggers
Source of infection: Rats
Characterized by fever, eschar, rash, and lymphadenopathy
Pathogen : Rickettsia tsutsugamushi

source of infection : chiggers,rats

clinical features:
•Incubation period: 4～21 days
•Sudden onset, High fever: remittent fever accompanied by chill, headache, malaise,
prostration, poor appetite.
Signs of multiorgan damage:
•Meningoencephalitis: delirium, convulsion, coma, and neck stiffness.
•Interstitial pneumonia: cough, chest pain, breathlessness.
Signs of multiorgan damage:
• Myocarditis: gallop rhythm, poor quality heart sounds, systolic murmurs.
• Hepatitis: jaundice, hemorrhage. Natural course: 2～3 weeks.

1. Eschar and ulceration:

• Characteristic sign.
• Seen in 36.9～98％ of patients.
• Generally located in warm, wet, intense smelled areas.

2. Lymphadenopathy:
• Enlarged markedly regional lymph nodes near the eschar.
• Generalized lymphadenopathy.
• Painful, movable, not purulent.

3. Rash:
• Appears on the 4th to the 6th day.
• Beginning on the trunk, spread to the extremities.
• Maculopapular, congestive, no itching.
• Lasting 3～7 days.
• Seen in 35～100％ of patients.

4. Splenomegaly and hepatomegaly

Splenomegaly :
30～50％ of patients.
Hepatomegaly:
10～20％ of patients.

covid
transmission : Respiratory transmission, Aerosol transmission, Fomite transmission, Faecal-oral
transmission, Transmission via other body fluids, Perinatal (vertical) transmission, Nosocomial
transmission.

chartacteristics of ct in covid : Bilateral focal consolidation. Lobar consolidation. Patchy

consolidation. Bilateral diffused patchy and fuzzy shadows.

high risk people for covid : Age >65. Multiple Medical Conditions (e.g., diabetes, chronic kidney
disease, obesity. lung disease, pregnancy). Unvaccinated. Immunocompromised.
bacillary dysentery
source of infection : shigella. S. dysenteriae, S. flexneri, S. boydii, S. sonnei

clinical features of bacillary decentart

ACUTE
- : ≤ 2months
- Typical type
- Acute onset begins within 24-48h. (Abdominal cramps, Dysentery, Tenesmus)
- Mild type
- Low or no fever. Diarrhea < 10 times/day. Mucoid but no bloody stools.
- Toxic type
- High fever, T>40°C, Restlessness. Generalized toxicity, sepsis, toxic shock, toxic encephalitis.
- Including 3 subtypes: shock type, cerebral type, and mixed type.
CHRONIC
- ≥ 2months
- Uncommon
- Malnourished infants or AlDs
- Abdominal pain, diarrhea, stool with blood, mucus, constipation, malnutrition, anemia, fatigue.

how long course of chronic dysentery : ≥ 2months

drug of choice to treat for adults

Adult: Quinolones ( IV by drip)
Ciprofloxacin, ofloxacin, gatifloxacin.

definitions
1.covert infection: Covert infections occur when bees have the virus under control, such that they do
not display symptoms of the disease, and are minimally or not at all affected by it.

2. scrap typhus : Acute febrile infectious disease caused by Rickettsia tsutsugamushi and Transmitted
by the bite of chiggers. Source of infection: Rats. Characterized by fever, eschar, rash, and
lymphadenopathy.

3.post infection immunity : exposure to a disease organism triggers the immune system to produce
antibodies to that disease,which help us protect ourselves from getting it again.

4.bacillary dysentery: Shigellosis is an intestinal infection caused by a genus of bacteria known as

Shigella that causes diarrheal disease of the colon or large intestines.

Diagnosrtic of SIRS

4 steps:
1. General condition
2. SIRS
3. Source of infection
4. Organ function

1. General condition
- Airway Breathing: RR, Distress, Pulse oximetry
- Circulation: HR, BP, Skin, JVP
- ABGS, Arterial lactasis.

2. SIRS
- HR(>90/min)
- RR(>20/min) or Paco2 <32 mmHg
- T (>38 °C or <36°C)
- WBC (>12000 mm-3 or < 4000 mm-3)
- CBC, WBC differential

3. Source of infection
- Respiratory (pneumonia, empyema)
- Abdominal (peritonitis, abscess, cholangitis)
- Skin(cellulitis, fasciitis)
- Pyelonephritis
- CNS (meningitis, brain abscess)
- C&S Gram stain, blood, sputum, urine, CSF
- CXR
- U/S, CT scan

4. Organ function
- CNS
- Renal function
- Liver function
- Gl function
- Respiratory function
Clues to a septic shock - Hypotension, oliguria or anuria
- Thrombocytopenia or bleeding
- serum lactate dehydrogenase increases, liver and kidney function abnormal

The test consists of 40 multiple choice questions, 10 judgment questions, 4 noun explanations, 4 short
answer questions, and 1 case analysis question