Infectious Diseases

1- a 24 yrs old pt. came for check up after a promiscuous relation 1 month ago .. he was
clinically unremarkable, VDRL : 1/128 … he was allergic 2 penicillin other line of
management is :combination is :
a- ciprofloxacin & metronedazole

Investigations for diagnosis

Treponema pallidum is not amenable to in vitro culture – the most sensitive and specific method is identification by
darkground
microscopy. Organisms may be found in variable numbers, from primary chancres and the mucous patches of
secondary lesions. Individuals with either primary or secondary disease are highly infectious.Serological tests used in
diagnosis are either treponemalspecific or non-specific (cardiolipin test) (Table 4.50):

■ Treponemal specific. The T. pallidum enzyme immunoassay (EIA). T. pallidum haemagglutination or particle
agglutination assay (TPHA/TPPA) and fluorescent treponemal antibodies absorbed (FTA-abs) test are both highly
specific for treponemal disease but
will not differentiate between syphilis and other treponemal infection such as yaws. These tests usually remain positive
for life, even after treatment.

■ Treponemal non-specific. The Venereal Disease Research Laboratory (VDRL) and rapid plasma regain (RPR) tests
are non-specific, becoming positive within 3–4 weeks of the primary infection. They are quantifiable tests which can be
used to monitor treatment efficacy
and are helpful in assessing disease activity. They generally become negative by 6 months after treatment in early
syphilis. The VDRL may also become negative in untreated patients (50% of patients with late-stage syphilis) or remain
positive after treatment in late stage.
False-positive results may occur in other conditions – particularly infectious mononucleosis, hepatitis, Mycoplasma
infections, some protozoal infections, cirrhosis, malignancy, autoimmune disease and chronic infections.
2- a 25 yrs old Saudi man presented with Hx of mild icterus , otherwise ok .. hepatitis screen :
HBsAg +ve , HBeAg +ve , anti-HBcAg +ve (this should be core anti body, because core
antigen doesn’t leave hepatocyte to the blood "prof. Yasawi" ) , the diagnosis :
a- acute hepatitis B
b- convalescent stage of hep. B
c- recovery with seroconversion Hep . B
d- Hep B carrier
e- chronic active Hep. B
Investigations
Specific tests. The markers for HBV are shown in Table 7.7. HBsAg is looked for initially; if it is found, a full viral profile is then performed. In
acute infection, as HBsAg may be cleared rapidly, anti-HBc IgM is diagnostic. HBV DNA is the most sensitive index of viral replication. HBV DNA
has been shown to persist (using polymerase chain reaction (PCR) techniques) even when the e antibody has developed.

(a) Acute infection

Antigens
HBsAg appears in the blood from about 6 weeks to 3 months after an acute infection and then disappears.
HBeAg rises early and usually declines rapidly.

Antibodies
Anti-HBs appears late and indicates immunity.
Anti-HBc is the first antibody to appear and high titres of IgM anti-HBc suggest an acute and continuing viral replication. It persists for many
months. IgM anti-HBc may be the only serological indicator of recent HBV infection in a period when HBsAg has disappeared and anti-HBs is not
detectable in the serum.
Anti-HBe appears after the anti-HBc and its appearance
relates to a decreased infectivity, i.e. a low risk.

(b) Development of chronic hepatitis followed by seroconversion

HBsAg persists and indicates a chronic infection (or carrier state).
HBeAg persists and correlates with increased severity and infectivity and the development of chronic liver disease. When anti-HBe develops
(seroconversion) the Ag disappears and there is a rise in ALT.
HBV DNA suggests continual viral replication.

3-What is the least effective AB of the following to staph. aureus:

• clindamycin.
• erythromycin.
• amoxicillin.
• Vancomycin.

Fewer than 5% of staph. aureus isolates are sensitive to penicillin.

- Which of the following antibiotics has the least activity against S. aureus?
a. Erythromycin.
b. Clindamycin.
c. Vancomycin.
d. Dicloxicillin.
e. First generation cephalosporins.

4- regarding protective measures of malaria, all true except:

- infestation occur more in day than night :
- using insect repellant is useful

5- Regarding typhoid fever, all are true except:

• fever and red spots appear on the same time.
• can be completely eradicated even in the presence of gall stones.
• transmitted by food, milk and water.
• can be treated by quinolones.

Early physical findings of enteric fever include rash ("rose spots"), hepatosplenomegaly (3–6%),
epistaxis, and relative bradycardia at the peak of high fever.

The 1–5% of patients who develop chronic carriage of Salmonella can be treated for 4–6 weeks
with an appropriate oral antibiotic. Treatment with oral amoxicillin, trimethoprim-sulfamethoxazole
(TMP-SMX), ciprofloxacin, or norfloxacin is ~80% effective in eradicating chronic carriage of
susceptible organisms. However, in cases of anatomic abnormality (e.g., biliary or kidney stones),
eradication often (not always) requires both antibiotic therapy and surgical correction.

6- Within 6 hours after attending a dinner party, 10 participants developed sever N/V,
abdominal cramp and diarrhea. Most of them resolved spontaneously. Few were admitted for
correction of dehydration. The most probable cause is:
a. Salmonella food poisoning.
b. Botulism.
c. Staphylococcal food poisoning.
d. Giardiasis.
e. Clostridium perfringes food poisoning.

-A family went to a dinner party after 6 hours they all had symptoms of abdominal
pain,nausea, vomiting and dehydration. Some of them recovered while others needed
hospitilzation. What’s the most likely organism?
a) giardia
b) staph aurens
c) salmonella
d) c . perfiringis
e) c.boyulism
 Bacterial Food Poisoning
Incubation Period, Common Food Sources
Symptoms
Organism

1–6 H

Nausea, vomiting, diarrhea Ham, poultry, potato or egg

Staphylococcus aureus salad, mayonnaise, cream
pastries
Bacillus cereus Nausea, vomiting, diarrhea Fried rice

8–16 H
Beef, poultry, legumes,
Clostridium perfringens Abdominal cramps, diarrhea gravies
(vomiting rare)
Abdominal cramps, diarrhea Meats, vegetables, dried
B. cereus
(vomiting rare) beans, cereals

>16 H
Vibrio cholerae Watery diarrhea Shellfish
Enterotoxigenic
Watery diarrhea Salads, cheese, meats, water
Escherichia coli
Ground beef, roast beef,
Enterohemorrhagic E. coli Bloody diarrhea salami, raw milk, raw
vegetables, apple juice
Beef, poultry, eggs, dairy
Salmonella spp. Inflammatory diarrhea
products
Campylobacter jejuni Inflammatory diarrhea Poultry, raw milk
Potato or egg salad, lettuce,
Shigella spp. Dysentery
raw vegetables
Vibrio parahaemolyticus Dysentery Mollusks, crustaceans

7- The following are characteristics features of brucellosis except:

a. Lymphadenopathy
b. Hepatomegly.
c. Splenomegaly.
d. Diarrhea.
e. Backache.

- All symptoms and signs of brucellosis, except:

• Back pain. • Lymphadenopathy
• Splenomegaly • Hepatomegaly
• Gastroenteritis

Clinical Features An incubation period of 1 week to several months is followed by the

development of undulating fever; sweats; increasing apathy, fatigue, and anorexia; and nonspecific
symptoms such as headache, myalgias, and chills.

Brucellosis often presents with one of three patterns:

1. a febrile illness similar to but less severe than typhoid fever;
2. fever and acute monarthritis, typically of the hip or knee, in a young child (septic arthritis);
or
 3. long-lasting fever and low back or hip pain in an older man (vertebral osteomyelitis).

In an endemic area (e.g., much of the Middle East), a patient with fever and difficulty walking
into the clinic would be regarded as having brucellosis until it was proved otherwise.

Brucella infection can cause lymphadenopathy, hepatosplenomegaly, epididymoorchitis, neurologic

involvement, and focal abscess.

8- in brucellosis, all of the following are true except:

a) brucella abortus cause more severe form than B. melitansis in children .
b) human to human is rarely documented .
c) human can be infected through inhalation .
d) brucella species are small, non motile gram -ve coccobacilli .
e) pt with high titer can show false -ve .
The organisms usually gain entry into the human body via
the mouth; less frequently they may enter via the respiratory
tract, genital tract or abraded skin.

ETIOLOGY
Human brucellosis can be caused by any of four species:
1. Brucella melitensis (the most common and most virulent cause of brucellosis worldwide) is
acquired primarily from goats, sheep, and camels;
2. B. abortus from cattle;
3. B. suis from hogs; and
4. B. canis from dogs.
These small aerobic gram-negative bacilli are unencapsulated, nonmotile, non-spore-forming, facultative
intracellular parasites that cause lifelong infection in animals. Brucellae are killed by boiling or pasteurization
of milk and milk products. They survive for up to 8 weeks in unpasteurized, white, soft cheese made from
goat's milk and are not killed by freezing. The organisms remain viable for up to 40 days in dried soil
contaminated with infected-animal urine, stool, vaginal discharge, and products of conception and for longer
periods in damp soil.

Brucella abortus (cattle), B. melitensis (goat/sheep), B. suis (swine), and B. canis (dog) are the most
common organisms responsible for human disease. These organisms are small, aerobic, non-spore-forming,
nonmotile, gram-negative coccobacillary bacteria that are fastidious in their growth but can be grown on
various laboratory media including blood and chocolate agars. When brucellosis is suspected, however, the
clinical laboratory should be alerted so the cultures can be maintained for ≥21 days to ensure growth if the
organism is present.

DIAGNOSIS.
1. Routine laboratory examinations of the blood are not helpful; thrombocytopenia, neutropenia,
anemia, or pancytopenia may occur. A history of exposure to animals or ingestion of unpasteurized
dairy products may be more helpful.
2. A definitive diagnosis is established by recovering the organisms in the blood, bone marrow, or other
tissues. Although automated culture systems and the use of the lysis-centrifugation method have
shortened the isolation time from weeks to days, it is prudent to alert the clinical microbiology
laboratory that brucellosis is suspected. Isolation of the organism still may require as long as 4 wk
from a blood culture sample.Caution is also advised when using automated bacterial identification
systems, because isolates have been misidentified as other gram-negative organisms (Haemophilus
influenzae type b).
3. In the absence of positive culture results, various serologic tests have been applied to the
diagnosis of brucellosis. The serum agglutination test (SAT) is the most widely used and detects
antibodies against B. abortus, B. melitensis, and B. suis. This method does not detect antibodies
against B. canis because this organism lacks the smooth lipopolysaccharide. No single titer is ever
diagnostic, but most patients with acute infections have titers of ≥1 : 160. Low titers may be found
early in the course of the illness, requiring the use of acute and convalescent sera testing to confirm
 the diagnosis. Because patients with active infection have both an immunoglobulin M (IgM) and an
IgG response and the SAT measures the total quantity of agglutinating antibodies, the total quantity
of IgG is measured by treatment of the serum with 2-mercaptoethanol. This fractionation is important
in determining the significance of the antibody titer because low levels of IgM can remain in the
serum for weeks to months after the infection has been treated. It is important to remember that all
titers must be interpreted in light of a patient's history and physical examination. False-positive
results due to cross-reacting antibodies to other gram-negative organisms such as Yersinia
enterocolitica, Francisella tularensis, and Vibrio cholerae can occur. In addition, the prozone effect
can give false-negative results in the presence of high titers of antibody. To avoid this issue,
serum that is being tested should be diluted to ≥1 : 320.
4. Among newer tests, the enzyme immunoassay appears to be the most sensitive method for
detecting Brucella antibodies.
5. Polymerase chain reaction assays are also becoming available but at this time are mostly limited
to research facilities.

9- 82 y/o female presented to ER in confusion with hypotension. BP was 70/20, P=l6O/min,

rectal T= 37.7°C. The most likely of the following would suggest sepsis as a cause of
hypotension is:
a- Low systemic vascular resistance & high cardiac output.
b- High systemic vascular resistance & low cardiac output.
c- Pulmonary capillary wedge pressure less than 26.
d-PH is less than 7.2.
e- Serum lactate dehydrogenase more than 22.
Septic shock is characterized by a decrease in peripheral vascular resistance despite increased
levels of vasopressor catecholamines. Although blood flow to peripheral tissues increases, oxygen
utilization by these tissues is greatly impaired.

CLINICAL FEATURES
 Hyperventilation
 Encephalopathy (disorientation, confusion)
 Acrocyanosis, ischemic necrosis of peripheral tissues (e.g., digits) due to DIC
 Skin: hemorrhagic lesions, bullae, cellulitis. Skin lesions may suggest specific pathogens—
e.g., petechiae and purpura with Neisseria meningitidis, ecthyma gangrenosum in pts with
Pseudomonas aeruginosa.
 Gastrointestinal: nausea, vomiting, diarrhea, ileus, cholestatic jaundice

Major Complications
 Cardiopulmonary manifestations
 Ventilation-perfusion mismatch, increased alveolar capillary permeability, increased
pulmonary water content, and decreased pulmonary compliance impede oxygen exchange
and lead to acute respiratory distress syndrome (progressive diffuse pulmonary infiltrates
and arterial hypoxemia) in ~50% of pts.
 Hypotension: Normal or increased cardiac output and decreased systemic vascular
resistance distinguish septic shock from cardiogenic or hypovolemic shock.
 Myocardial function is depressed with decreased ejection fraction.
 Renal manifestations: oliguria, azotemia, proteinuria, renal failure due to acute tubular
necrosis
 Coagulopathy
 Neurologic manifestations: polyneuropathy with distal motor weakness in prolonged sepsis

Laboratory Findings
 Leukocytosis with a left shift, thrombocytopenia
  Prolonged thrombin time, decreased fibrinogen, presence of D-dimers, suggestive of DIC.
With DIC, platelet counts usually fall below 50,000/μL.
 Hyperbilirubinemia, increase in hepatic aminotransferases, azotemia, proteinuria,
hypoalbuminemia
 Metabolic acidosis, elevated anion gap, elevated lactate levels, hypoxemia

10-A 55 years old male with COPD , complaining of 1 wk fever and productive cough on CXR
showed Left upper pneumonia, sputum culture +ve for H.inf, most drug effective is
a. Pencillin
b. Doxycycline
c. Cefuroxime
d. Gentamycin
e. Carbinacillin

- A 55 years old man known case of COPD. Now complaining of 1 week fever, productive
cough. CXR showed left upper lobe pneumonia. Sputum culture positive H.influenza. what
are you going to give him?
a- penicillin.
b- doxycyclin.
c- cefuroxirne.
d- gentamycin.
e- carbincillin

Haemophilus influenzae produces beta lactamases, and it is also able to modify its penicillin
binding protein, so it has gained resistance to the penicillin family of antibiotics. In severe cases
cefotaxime and ceftriaxone are the elected antibiotics, delivered directly into the bloodstream, and
for the less severe cases an association of ampicillin and sulbactam, cephalosporins of the second
and third generation, or fluoroquinolones.
Many infections caused by nontypable strains of H. influenzae, such as otitis media, sinusitis, and
exacerbations of COPD, can be treated with oral antimicrobial agents. Approximately 25% of nontypable
strains produce -lactamase and are resistant to ampicillin. Infections caused by ampicillin-resistant strains
can be treated with a variety of agents, including trimethoprim-sulfamethoxazole, amoxicillin/clavulanic acid,
various extended-spectrum cephalosporins, and newer macrolides (azithromycin and clarithromycin).
Fluoroquinolones are highly active against H. influenzae but are not currently recommended for the
treatment of children or pregnant women because of possible effects on articular cartilage.

11-Which one of the following diseases is not transmitted by mosquitoes?

a)rift valley fever
b)yellow fever
c)relapsing fever
d)filariasis
e)dengue fever

Rift Valley fever is transmitted by mosquitoes and is usually amplified in ruminant hosts. In endemic regions, cases
can occur sporadically or in epidemics. The virus appears to survive in the dried eggs of Aedes mosquitoes; epidemics
are associated with the hatch-ing of these mosquitoes during years of heavy rainfall and localized flooding. In Africa,
outbreaks typically occur in savannah grasslands every 5 to 15 years, and in semi-arid regions every 25 to 35 years.
Once it has been amplified in animals, the RVF virus can also be transmitted by other vectors, including many mosquito
species and possibly other biting insects such as ticks and midges. The virus can be transmitted in utero to the fetus. It
.has also been found in semen and raw milk
Humans do not seem to be infected by casual contact with live hosts, but can be in-fected by aerosols or direct
contact with tissues during parturition, necropsy, slaughter, laboratory procedures or meat preparation for cooking. In
.utero transmission to a human infant was first reported in 2006
Both animals and humans theoretically have the potential to introduce Rift Valley fe-ver into new areas by
.infecting mosquitoes

Yellow fever is an acute viral hemorrhagic disease. The yellow fever virus is mainly transmitted
through the bite of the yellow fever mosquito Aedes aegypti, but other mosquitos such as the " tiger
mosquito" (Aedes albopictus) can also serve as a vector for the virus.

Relapsing fever (synonym: typhinia[1]) is an infection caused by certain bacteria in the genus
Borrelia.[2] It is a vector-borne disease that is transmitted through louse or soft-bodied tick bites.[

Filarial nematodes enter the human body at their third larval stage by escaping from the mouthparts
of their vector arthropod as they bend during biting and enter through the bite wound in the skin.

Dengue is transmitted to humans by the Aedes aegypti or more rarely the Aedes albopictus
mosquito, which feed during the day.[6

12- Pt presents with fever swelling is felt,Ant.lymph node swelling warm, tender & fluctuant
Dx:
a) viral infection .
b) bacterial lymphadenitis .
c) Hodgkin L.
d) ALL .

Lymphadenitis typically causes pain, tenderness, and lymph node enlargement. Pain and tenderness
typically distinguish lymphadenitis from lymphadenopathy. With some infections, the overlying
skin is inflamed, occasionally with cellulitis. Abscesses may form, and penetration to the skin
produces draining sinuses. Fever is common.
13- Patient with H/O fever, peripheral blood film +ve for malaria:
a) Banana shaped erythrocyte is seen in P. vivax
b) Mostly due to P. falciparium
c) Treated immediately by primaquin 10mg for 3 days
d) Response to Rx will take 72 hr to appear
Known chloroquine-sensitive strains of Plasmodium vivax, P. malariae, P. ovale, P. falciparuma
Chloroquine (10 mg of base/kg stat followed by 5 mg/kg at 12, 24, and 36 h or by 10 mg/kg at 24 h and 5 mg/kg at 48 h)
or
Amodiaquine (10–12 mg of base/kg qd for 3 days)
Radical treatment for P. vivax or P. ovale infection In addition to chloroquine or amodiaquine as detailed above, primaquine (0.25 mg of base/kg qd;
0.375–0.5 mg of base/kg qd in Southeast Asia and Oceania) should be given for 14 days to prevent relapse. In mild G6PD deficiency, 0.75 mg of
base/kg should be given once weekly for 6 weeks. Primaquine should not be given in severe G6PD deficiency.
14-The following drugs can be used in prophylaxis of malaria in chlorquine-resistant area,
except:
a) Mefloquin .
b) Doxycycline .
c) Proguanil .
d) Chlorquine + dapsone + pyrimethamine .
Atovaquone/proguanil (Malarone) Prophylaxis in areas with chloroquine- or mefloquine-resistant Plasmodium falciparum

Doxycycline Prophylaxis in areas with chloroquine- or mefloquine-resistant P. falciparumc

- the following can be used in prophylaxis in malaria in chlorquine resistant area except:
a-mefloquine
b-doxycycline
c-chlorquine with proguanil
e-dapsone

15- Hepatitis most commonly transferred by blood is:

a) HBV.
b) HAV.
c) HCV (previously known as non a non b).
d) None of the above.
16- The greatest risk of developing chronic hepatitis and cirrhosis occurs after:
a. Hepatitis A infection.
b. Hepatitis B infection.
c. Hepatitis C infection.
d. Hepatitis D infection.
e. Hepatitis E infection.

Hepatitis B infection Course

The majority of patients recover completely, fulminant hepatitis occurring in up to 1%. Some patients go on to develop
chronic hepatitis (p. 338), cirrhosis (p. 345) and hepatocellular carcinoma (p. 363) or have inactive chronic HBV
infection (Fig. 7.17). The outcome depends upon several factors, including the virulence of the virus and the
immunocompetence and age of the patient. Some genetic factors, e.g. the presence of MHC class II genotype, may alter
host defence to HBV. Complete eradication of HBV infection is probably rare.

Hepatitis C infection Course

Eighty five to ninety per cent of asymptomatic patients develop chronic liver disease. A higher percentage of
symptomatic patients ‘clear’ the virus with only 48–75% going on to chronic liver disease (p. 341). Cirrhosis develops
in about 20–30% within 10–30 years and of these patients between 7% and 15% will develop hepatocellular carcinoma.
The course is adversely affected by co-infection with HBV and/or HIV, and by alcohol consumption, which should be
discouraged.
17- In a gram-negative bacterial septicemia:
a) pseudomonas is the most common organism involved.
b) Many of the advese changes can be accounted for by endotoxin.
c) The cardiac index is low
d) Central venous pressure is high.
e) Endotoxin is mainly a long-chain peptide.

Lipopolysaccharide (LPS, also called endotoxin) is the most potent and best-studied gram-negative
bacterial signal molecule.
Endotoxin is a lipopolysaccharide (LPS) derived from the cell wall of Gram-negative bacteria and is a potent trigger of
the inflammatory response.
Approximately two-thirds of cases occur in patients hospitalized for other illnesses. The increasing incidence
of severe sepsis in the United States is attributable to the aging of the population, the increasing longevity of
patients with chronic diseases, and the relatively high frequency with which sepsis develops in patients with
AIDS.
Blood cultures are positive in 20–40% of sepsis cases and in 40–70% of septic shock cases. Of cases with positive
blood cultures, a single gram-positive or gram-negative bacterial species accounts for ~70% of isolates; the remainder
are fungi or a mixture of microorganisms.

Cardiac index (CI) is a vasodynamic parameter that relates the cardiac output (CO) to body
surface area (BSA),[1] thus relating heart performance to the size of the individual. The unit of
measurement is litres per minute per square metre (l/min/m2).
Calculation
The index is usually calculated using the following formula:

where
CI=Cardiac index
BSA=Body surface area
SV=Stroke volume
HR=Heart rate
CO=Cardiac output

Fluid-resistant septic shock secondary to central venous catheter-associated infection was typically
"warm shock" (15 of 16 patients; 94%), with high cardiac index and low systemic vascular
resistance index. In contrast, this pattern was rarely seen in community-acquired sepsis (2 of 14
patients; 14%), where a normal or low cardiac index was predominant.

18- In septic shock:

a) The mortality rate is 10 to 20%.
b) Gram-negative organisms are involved exclusively
c) The majority of patients are elderly
d) The most common source of infection is alimentary tract.
e) Two or more organisms are responsible in the majority of cases.

Sepsis is a disease seen most frequently in elderly persons and in those with comorbid conditions
that predispose to infection, such as diabetes or any immunocompromising disease. The latter are at
especially high risk, including those with cancer on chemotherapeutic agents, those with end-stage
renal or liver disease, those with advanced HIV, or those on steroids for any other
immunocompromising agent for chronic conditions. Patients with indwelling catheters or devices
are also at high risk.
the incidence of sepsis has increased 3-fold, between 1979 and 2000, from 83 cases to 240 cases per
year per 100,000 population. The reasons for this likely include an increasingly elderly population,
increased recognition of disease, increased performance of invasive procedures and organ
transplantation, increased use of immunosuppressive agents and chemotherapy, increased use of
indwelling lines and devices, and increase in chronic diseases such as end-stage renal disease and
HIV. Of note, in 1987, gram-positive organisms surpassed gram-negative organisms as the most
common cause of sepsis, which holds true today.9

The mortality rate from septic shock is approximately 50%

The mortality rate from sepsis is approximately 40% in adults, and 25% in children.[2]
Approximately 70% of septic shock cases were once traceable to Gram staining gram-negative
bacilli that produce endotoxins35% of septic shock cases derive from urinary tract infections, 15%
from the respiratory tract, 15% from skin catheters (such as IVs); over 30% of all cases are
idiopathic in origin.

21- HSV type 1 infection of the oral cavity, all true except:
a- Is the commonest viral infection in the oral cavity
b- Can give gingivostomatitis
c- In primary infection, there is systemic involvement
d- May present with tonsillitis without oral lesion
32- A 40 year old white male is transferred to your institution in septic shock less than 24
hours after onset of symptoms of a non-specific illness. He underwent a splenectomy for
trauma 5 years ago. Antibiotic coverage must be directed against:
a. Streptococcus, group A.
b. Klebsiella pneumoniae.
c. Staphylococcus aureus.
d. Escherichia coli.
e. Streptococcus pneumoniae.