Bacterial infection and Viseral leishmaniasis

Diphtheria

Dr.hussein K.H. Alatabi
MBChB,DCH,FICMS,CABP

Diphtheria

Diphtheria: is an acute infectious disease caused by corynebacterium diphtheriae and affects primarily the membranes of the upper respiratory tract with the formation of a gry- white pseudomembrane.
The causative organism,C.diphtheriae,is gram- positive pleomorphic bacillus.
The majority of cases occure during the cooler autuman and winter months in individuals younger than 15 years of age who are unimmunized.

pathophysiology

The single known reservoir for C.diphtheriae is humans;disease is acquired by contact with either acarrier or adiseased person.
The initial entry site for c. diphtheriae is via airborne respiratory droplets,typically the nose or mouth,but occasionally the ocular surface, the genital mucous membranes or preexisting skin lesions.following 2 to 4 days of incubation at one of these sites,the bacteria elaborates toxin.Locally the toxine induces formation of anecrotic coagulation of the mucous membranes (pseudomembrane) with underlying tissue edema,Respiratory compromise may ensue.Elaborated toxin may alsohave profound effects on the heart,nerves,and kidneys in the form of myocarditis,demyelination and tubular necrosis, respectively

Associated illnesses

Respiratory tract diphtheria:
Nasal diphtheria;usully in infants,starts as mild rhinorrhea then mucopurulent.
Tonsilar and pharyngeal diphtheria; begins with anoroxia,malaise,fever and pharyngitis. Amembrane appears within 1 to 2 days,cervical lymphadenitis and edema of soft cervical soft tissues may be severe.
Laryngeal diph.:represents extension of pharyngeal infection and clincally presents as typical croup
Cutaneous diph.: chronic non healing ulcers,in warmer tropical regions.
Other sites:rare;vulvovaginal,conjunctival or aural forms.


Complications
Cardiac toxicity:myocarditis may occure. Cardiac failure,the majority of cases are transient.
Neurologic toxicity: bilateral motor involvement.
Paralysis of soft palate is most common,but ocular paralysis,diaphram paralysis,peripheral neuropathy also occur.

Prognosis

Depend on:
Immunization status of the host.those without prior adequate immunization have high morbidity and mortality rate.
Delay in onset of treatment
Organism virulence
Location of membrane;laryngeal diph. has higher mortility
Amegakaryocytic thrombocytopenia and WBC<25,000 associated with poor outcome.

Data Gathering

∙Incubation period is 1 to 6 days.Respiratory diph. ,depending on the site of infection,may begin with nasal discharge alone or with pharyngitis accompanied by mild systemic symptoms.
▀ Physical examination :
nasal discharge, pharyngeal membrane (pseudomembrane) ,respiratory distress,stridor,cervical lymphadenitis .Attempts to remove any membrane present will result in bleeding.

Laboratory Aids

Diagnosis should be on clinical grounds.
Culture of material from membrane or beneath the membrane,examination of methylene blue-stained specimen( somtime spead identification)
Fluorescent antibody testing and counter immuno electrophoresis.


Therapy
Diphtheria antitoxin(DAT):
Pharyngeal or laryngeal disease of <48 hours duration,20,000 to 40,000 units IV
Nasopharyngeal lesions,40,000 to 60,000 units IV
Extensive diease of 3 or more days duration or diffuse neck swelling,80,000 to 100.000 units IV
Antibiotic therapy:
Should be used in addition to DAT as follows:
Respiratory diph.:-Penicillin G-Aqueous crystalline,100,000 to 150,000 u per Kg per day. -Procaine penicillin.—Erythromycin 40 to 50 mg per day orally or parenterally. For 14 days
Cutaneous diph.:local care and antimicrobials.
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Pertusis

Dr.Hussein K. H. Alatabi
M.B.Ch.B.,DCH,F.I.C.M.S,C.A.B.P.

Pertusis

One of highly commmunicable diseases with attaks rate close to 100% in susceptible individuals.
1st discription of disease in epidemic in paris in 1578.
Adisease of young children,the infants either nonimmunized or partialy immunized.
The disease in adolescents and adults is not usully recognized(now the major sourse of infection in children).


Pathophysiology
Bordetella pertusis is small,non motile,fastidious,gram-negative rode,replicates only in association with ciliated epithelium, causing congestion and inflammation of bronchi;peribronchial lymphoid hyperplasia followed by anecrotizing process occurs and results in bronchopneumonia:atelectasis can occur as aresult of bronchiolar obstruction from accumulated secretions.
Long incubation period( 7 to 21 days).
Apnea is acommon manifestation in young infants, less than 6 months of age.The characteristic (whoop) is typically abscent.
Rout of spread includes aerosolized respiratory droplets,direct contact with nasal secretions,and indirect contact with secretions through hand contact.

complications

Pneumonia,the most frequent complication,is responsible for more than 90% of deaths in young children with pertusis,and usually owing to secondary bacterial disease rather than B.pertusis itself.
Super infections as aresult of viruses(adeno v., RSV,CMV)or bacteria(setrepto,staph. And gram negative.)
Other pulmonary complications include atelectasis,pnemothorax,pnumomediastinum, and subcutaneous emphysema.
Seizures(3%)and encephalopathy(1%),may be related to fever.

Differential Diagnosis

B.parapertussis and adenoviruses
B.perussis
Bronchiolitis
Bacterial pneumonia
Cystic fibrosis
Tuberculosis
Foreign body aspiration
Prognosis:directly related to patient age;the highest mortality is observed in infants<6 months of age


Data Gathering
History:
Three stages:
Catarrhal stage(1 to 2 weeks);with symptoms of upper respiratory infection.
Paroxysmal stage(2 to 4 weeks or longer); characterized by paroxysmal cough with increased severity and frequency producing the characteristic whoop during the sudden forceful inspiratory phase;posttussive vomiting is also observed during this stage.
The convalscent stage begins and lasts 1 to 2 weeks but cough can persist for several months.

Physical examination

Rhinorrhea,lacrimation,conjunctival hyperemia ,and fever seen in early stage of disease.
Cyanosis observed during the paroxysmal stage.
Lung ausculatory examination is usully normal unless significant atelectasis or pneumonia has occurred.

Laboratory Aids

CBC;leukocytosis with predominant lymphocytosis(77 %) is commonly observed at the end of catarrhal stage and throughout the paroxysmal stage of illness.although this phenomenon is not frequently observed in infants.
Chest radiograghs: may reveal prehilar infiltrates or shaggy right heart border,(can be seen in other repiratory infections.
Culture and isolation of B.pertussis
Direct immunofluorescent assay of nasopharyngeal specimens.
Polymerase chain reaction(PCR)
Recntly developed monoclonal immunofluorescent antibody(BL-5)

Therapy

Patients with severe disease manifestations( apnea,cyanosis,feeding difficulties)or other complications require hospitalization for supportive care.
If antiboitic treatment is initiated during the catarrhal stage,it can prevent disease from progressing.Antibiotic have not been shown to shorten the course of illness if it begun during the paroxysmal stage.although it will elminate the organism from the nasopharynx withen 2 to 3 days,thus shortening the pontential for contagion.
Erythromycin(50 mg/kg per day) in 4 doses for 14 days
Newer macrolides;Azothromycin and clarithromycin, may be effective in shorter courses of 5 to 7 days.
Trimethoprim-sulamethoxazole another alternative
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DR.HUSSEIN K. H. ALATABI
MBCHB,DCH,FICMS,CABP
Tetanus

Tetanus

Adisease characterized by tonnic spasms of skeletal muscles and occasionally the glottis and larynx as aresult of intoxication with an exotoxin tetanospasmin prodused by clostridium tetani.
C.tetani is gram positive rod found in superficial layers of soil,specially in agricultural areas.
Tetanus,espeecially neanatal tetanus remain amajor problem in developing countries.
Incubation period usully 3 to 21 days,some cases reported with shorter period or it may be long as several months.

Complications

Most complications are related to the sever tetanic muscle contractions;
Sever spasm of the paraspinal lead to compression fracture of vertabral bodies.
Spasm of the chest wall and laryngospasm may precipitate respiratory failure and arrest.
Spasm may cause dysphagia,hydrophobia,neck stiffness,and urinary retention
Cerebrovascular hemorrhages may be seen,but rare espcially in neonatal tetanus.
Pnuemonia,including aspiration may be acomplication.

Clinical features

Pain: local tetanus is associated with painful muscle cotraction,limited to area near the wound.which may progress to generalized tetanus.
Trismus:seen in about half of cases;dysphagia, neck pain and stiffness,restlessness and headache.
Neonatal tetanus; usully complicates deliveries in septic conditions,and the mother is either unimmunized or not up to her date immunization status


Physical Examination
Trismus:initial sign,persistent trismus give rise to the classic sardonic smile(wrinkling of the forehead and distortion of the eyebrows and the corners of the mouth).
Fever
Tetanus spasms stimulated by variety of stimui including acold draft,noise,pain,anxiety and light touch.
Tachycardia,flushing and hypertension

Diagnosis is made clinically,investigations of limited use as anaerobic wound cultures,the WBC normal or mildly elevated,EEG andEMG are non specific.

Therapy

Specific;
Human tetanus immuneglobulin(TIG)
Tetanus antitoxin(TAT),if TIG not available.
Penicillin G
Surgical debridement and wound care
Supportive:
Ventilatory and cardiovascular support in ICU
Patients should be kept in quiet,darkened room.
Tracheostomy,parenteral nutrition,….
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Scarlet fever

Dr.Hussein k.H.Alatabi
MBChB,DCH,FICMS,CABP


Scarlet fever
Aclinical syndrom consisting of fever, pharyngitis,cervical lymphadenitis and the characteristic(sand paper rash) which results from infection with astrain of setrptococcus pyogenes(group A B-hemolytic setrpto.)that elaborates setrpt. Pyrogenic toxin which include A,B and C, toxine A is associated with more virulent disease
Incubation period is usully 24-48 hours.
Peak incidence during 1st few school years.
Occurs commonly before the age of age 3 years or after the age of 15 years.
More common in temperate and cold climates and in winter and spring months.

Pathophysiology

Susceptible individualls thought to lack toxine specific immunity.
Rash and toxic features due to development of hypersensitivity to the toxin which therefore require prior exposure to the toxin.

Complications

Acute otitis media
Sinusitis
Supurative cervical lymphadenitis
Pneumonia with or without effusion/empyemia.
Peritonsillar cellulitis/abscess
Retropharyngeal abscess
Meningitis
Brain abscess
Thrombosis of intracranial venous sinuses
Osteomyelitis
Hepatitis
Arthritis
Acute rheumatic fever(ARF)
Acute post infectious glomerulonephritis(APGN)
Erythema nodosum(possibly)


Differential Diagnomosis
Non scarletinal sterptococcal pharyngitis/tonsilitis.
Viral exanthems(measles,Rubella, Erythema infectiosum)
Drug eruptions
Staphylococcal scalled skin syndrom(ssss)
Toxic epidermal necrolysis(TEN)
Toxic shock syndrom(strepto or staphylo.)
Kawasaki disease
Uncommon(mercury.Atropin,Rifampicin poisoning

Clinical features

Sudden onset of fever up to 40.5 cent.,sore throat,headache,nausea and vomiting.
Physical finding:
Fine maculopapular(sand paper texture) rash on erythematous background( texture important than appearance) usully begins on the trunk and spreads to involve almost all entire body within hours to days.
Deep,red,non blanching lesion in antecubital and popliteal areas called ( pastia lines)
Circumoral pallor(classic finding)
White coat of the dorsum of the tongue early in illness then desquamates and reveals swollen,red and mottled(strawberry tangue)
Phyranx and tonsils are beefy red and may contain exudates.
Homorrhagic spots on interior pillar of tonsils and soft palate.
Large tender lymph nodes.


Laboratory Aids
Rapid setrptococcal antigen test: 50-80% sensitivity and more than 95% specificity
Throat culture ;the best sensitivity(>90%) should be done when rapid test negative.
White blood cell count(WBC) usully elevated
Esinophilia; common in recovery phase,
Prognosis:
Excellent,few patients suffer suppurative complications.

Therapy

Therapy started and lasts as 9 days after illness onset and should be effective in preventing ARF
Oral penicillin V: 250 mg twice aday for 10 days.
IM benzathine penicillin G: 600,000 units for children less than 60 pounds and 1,200,000 units for larger children
Clarithromycin (15 mg/kg/day given every 12 hours.and Azothromycin(20mg/kg/day once adialy for 3 days.
Erythromycin,amoxicillin,clindamycin and 1st generation cephalosporine,….
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Viseral leishmaniasis(KALA-AZAR)

Dr.hussein K.H. Alatabi
MBCHB,DCH.FICMS.CABP

Aclinical syndrom caused by aprotozoan called(leishmania donovani).The vector of disease is asand fly called(phlebotomus).It is prevalent in north Africa,India,south Africa, south America and meditteranean coast.It is endemic in Iraq mainly in Dialah,Souwairah, Abo ghreab,Tarmiah,Nahrawan,…
Typically affects children younger than 5 years of age,so in mediterranean region called(L. infantum)
V.L. (KALA-AZAR)


The host usully dogs, The prasite become infected in gut of vector(phlebotomus) then to human.
Dog gut of vector human
Incubation period: 2-6 months (2-3 weeks up to 10 years.
Cycle of disease

Fever : Acute onset,temperature rises to fastigium in the first week.After afurther week or tow of remittent fever it may settle by lysis
In older child the onset is often insidious with lethrgy,headache and general malaise, fever irregular and may be continuous,remittent or intermittent.
Splenomegaly develops early and my reach enormous proportions.usully in association with hepatomegally.

Clinical features

Loss of weight, intercurrent infections, purpura,oedema,ascites,sever anaemia.
Acharacteristic pigmentation may occasionally develop over the forhead,nose, hands and feet,the hair becomes briittle and falls out, appetite usully stay good.
Clinical features(cont.)

CBC:anemia,leukopenia(neutropenia) and thrombocytopenia.

Elevated hepatic transaminase levels and hyperglobulinemia(mostly Ig G).
Smears or cultures of material from splenic, bone marrow or lymph nodes aspirations( diagnostic specilly splinic aspirate)
Serologic testing by enzyme immuno assay, indirect fluorescence assay, or direct agglutination is very usefull in(V.L.) becouse of very high level of antileishmanial antibodies.
Laboratory Aids


An enzyme-linked immunosorbent assy( ELISA) using arecombinant (K 39) antigen,has sensitivity and specifity close to 100 %
:Endemic area+pancytopenia+ hypergamaglobenemia+SM= KALAZAR
Comlications:-Concrum oris-jaundice –infection-post kalazar dermal leishmaniasis.,…….
Lab.Aids(cont,)

Antimony compounds(sodium stibogluconate ): 20 mg/kg IV or IM for 28 days,course can be repeated in case of clinical relapse(i.e after 2 months of completion treatment.)
Amphotericin B desoxycholate can be used in unresponsive cases.
Supportive tretment also required according to case.
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Treatment