RICKETTSIOSIS

Rickettsioses are group of acute infectious diseases caused by especial organisms - Rickettsia and transmitted by insects.

Rickettsioses of human are divided into five groups.

1. Typhus group - epidemic typhus (Louse-Borne typhus), Brill-Zinsser disease and the endemic typhus (Murine typhus).

2. Spotted fever group - Rocky Mountain spotted fever, Boutonneuse (Marseilles fever), North-Asian tick-borne typhus, Queensland tick typhus, rickettsialpox.

3. Tsutsugamushi group - scrub typhus.

4. Q-fever group.

5. The group of the paroxysmal rickettsioses - trench fever (volynian fever).

EPIDEMIC TYPHUS FEVER

Synonyms ~ jail fever,ship fever,putrid fever,petechial fever,typhus exan-thematicus.

Epidemic typhus fever is an acute infections disease caused by Rickettsia prowazekii. Epidemic typhus fever is characterized by development of generalized thrombovasculitis, meningoencephalitis, severe common intoxication, by appearance of rash, enlargened liver and spleen. It is transmitted by the lice, Pediculus humanus.

Historic reference

Epidemic typhus fever has been one of the great epidemic diseases of the world. Its history belongs to the dark pages of the world's story, at times when war, famine and misery of every kind are present.

The disease was first described with sufficient accuracy by Fracastoro, in the 16th century,to enable us distinctly to differentiate it from plaque; the stuporous states of the two disease having previously caused them to be confounded.

Epidemics of typhus have very frequently been associated with war. In fact, severe epidemics have occurred during practically every great war in Europe with the exception of the Franco-Prussion war in 1870. In the World War, the epidemic which raged in Serbia in 1915 was one of the most severe which has occurred in modern times. It was characterized not only by its high virulence and high mortality. During the epidemia the number of new fever cases entering the military hospitals alone, reached as high as 2,500 per day, and the number of reported cases among the civilian population was approximately three times was this number. The mortality during the epidemic varied during the epidemic at

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different periods in different localities between 30 and 60 %, and in complicated cases sometimes reached 70 %. Over 150,000 deaths occurred within 6 months, before the epidemic could be suppressed. An astonishing 30 million cases occurred in Russia and Eastern Europe during 1918-1922, with an estimated 3 million deaths. During World War II, typhus struck heavily in concentration camps in Eastern Europe and in North Africa.

In the present time this disease may be occurs in Africa (Burundi, Ethiopia), in the Central America (Mexico, Peru).

Etiology

The etiologic agent is Rickettsia prowazekii, an obligate intracellular bacterium that is closely related antigenically to the agent that causes murine typhus (Rickettsia typhi). The organism is cocobacillary but has inconstant morphologic characteristics. Reproduction is by binary fission and diplobacilli are produced that are frequently seen in tissue sections. Special staining (Giemsa) provides good visualization of the organisms in the cytoplasm of cells.

Epidemiology

The source of infection is a sick man. Epidemic typhus (Louse-Borne typhus) is transmitted from person to person by the body louse (Pediculus humanus corporis). The louse feeds on an infected, rickettsemic person. The organism in the louse infects its alimentary tract and results in large numbers of organisms in its feces within about 4-5 days. Close personal or clothing contact is usually required to transmit lice to others. When the louse takes a blood meal,it defecates. The irritation causes the host to scratch the site, thereby contaminating the bite wound with louse feces. Human infection might also occur by mucous membrane inoculation with contaminated louse feces.

Human conditions that foster the proliferation of lice are especially common during winter and during war or natural disasters - where clothing is not changed,crowding occurs,and bathing is very infrequent.

In epidemic the susceptibility is high for all age groups.

Pathogenesis

After local proliferation at the site of the louse bite, the organism spreads hematogenously. Rickettsia prowazekii, as with most rickettsia, produces a vasculitis by infecting the endothelial cells of capillaries, small arteries, and veins. The process results in fibrin and platelet deposition and then occlusion of the vessel. Perivascular infiltration with lymphocytes, plasma cells, histiocytes, and polymorphonuclear leukocytes occurs with or without frank necrosis of the vessel. The angiitis is most marked in the skin, heart, central nervous system, skeletal muscle, and kidneys.

The mechanism of the development of epidemic typhus may be represented by the next phases:

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1. Penetration of Rickettsia prowazekii into organism and reproduction in the endothelial cells of the vessels.

2. Destruction of endothelial cells and penetration of rickettsia into the

blood - rickettsiemia, toxinemia.

3. Functional violations of the vessels in all organs and tissues - vasodilatation, slowdown of the stream of the blood.

4. Destructive and proliferative alterations of the capillaries with formation specific granulemas (nodules).

5. Formation of immunity.

Anatomic pathology

Small hemorrhages in the conjunctivae are frequent. The heart usually shows slight gross changes. Microscopically the blood vessels show similar lesions to those observed in the skin, and sometimes there is considerable infiltration with mononuclear and polymorphonuclear cells. Thrombi are rarely found in the larger blood vessels.

The blood is usually dark colored and liver and kidneys show cloudy swelling. The spleen is somewhat enlarged during the early stages of the disease but tends to be normal in size later on. It is often very soft and then may rupture from being handled at autopsy. Microscopically, engorgement with blood, with extensive phagocytosis of red blood corpuscles and diminution of lymphoid elements, is commonly present.

The lesion in the brain, particularly in the basal ganglia, medulla and cortex of the cerebrum, and more rarely in the white matter and cerebellum, correspond in size to miliary tubercles and are secondary to lesions of the small blood vessels and capillaries, as in the skin. They first consist of a collection of large cells of vascular and perivascular origin, endothelium, and monosytes, with necrosis resulting from occlusion of the vessels.

Clinical manifestations

Epidemic typhus is cyclic infectious disease. There are the next periods in the course of the disease: incubation period (it's duration is from 6 till 25 days). Initial period till appearance of the rash (it's duration is 4-5 days), period of climax - from appearance of rash till normalization of the temperature (it's duration is from 4-5 days till 8-10 days) and period of reconvalescence (it's duration is 2-3 weeks).

After an incubation period an abrupt onset with intense headache chills, fever and myalgia is characteristic. There is no eschar. The fever worsens quickly and becomes unremitting and the patient is soon prostrated by the illness. Giddiness, backache, anorexia, nausea are observed in the patients. The appearance of the patient is typical. The face is edemaous, flushed. Eyes are brilliant with injected sclera ("rabbit's eyes"). Enanthema (small hemorrhages) on the basis of uvula is marked on the second-third day of the disease (symptom

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of Rosenberg). The petechial rash may be revealed on transitive folds of conjunctiva from the third-forth day (symptom of Kjary-Aucyne). The early sign is tremor of the tongue, it's declining to the side (symptom Govorov-Godeljae) due to bulbaric disorders. Splenomegaly is marked on the 3-4 day of the disease in the majority of the patients. ;

Climax period is characterized by development of all clinical manifestations of the disease. The temperature is definite high level (febris remittans). Temperature decreases frequently on the 3-4,8-9 and 12-13 day of the disease and than the temperature increases again. Climax period is accompanied with intoxication and damage of central nervous system.

The appearance of the rash is an important sign of climax period. A rash begins in the axillary folds and upper part of the trunk on about the fifth day of illness and spread centrifugally. Initially, the rash consists of nonconfluent, pink macules that fade on pressure, may be rose- and petechial like. Within several days, the rash becomes rnaculopapular, darker, petechial and confluent and involves the entire body, palms and soles but never the face. Disappear with decreasing of temperature.

Circulatory system. Very outspoken is cardiac weakness due to myocardial degeneration. The heart sounds are very weak and the pulse feeble, rapid and irregular. The blood pressure often is very low, especially the diastolic, and may remain so throughout the disease. Bradycardia may be marked during convalescence.

Respiratory system. Cough may appear in the first days, but usually is first troublesome about the time of the eruption. By the end of a week, the cough becomes loose and rales of various types may be noted.

Alimentary tract. Constipation is usually noted. Very marked is the tendency of the mouth and tongue to become dry and sordes to collect on the teeth. It is often difficult to get the patient to protrude his tongue when told to do so. In the patients with epidemic typhus splenomegaly and hepatomegaly (from one second week) are marked.

Nervous system. Clouding of the consciousness may be as marked in this disease. Dull aching frontal headache is common and is an early predominating symptom. It frequently diminishes before the eruption appears. A dull stuporous state soon comes on. Delirium is marked in some cases. There are often the faces and mental state of alcoholic intoxication. There may be meningitis, meningoencephalitis.

In epidemic typhus fever it may be leucocytosis, neutrophylosis, monocytosis in the blood. ESR is accelerated.

Variants of the disease course.

There are mild, medium serious and serious course of the epidemic typhus fever. During the light course of the disease the occurrences of intoxication are expressed insignificantly. The temperature increases till 38 °Ñ. The consciousness

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is no changed. The rash predominates as roseoles. The liver and spleen increases in a third of patients. The duration of fever is till ^9 days. The mild course is observed in 10-20 % patients.

The medium serious course of the disease occurs more frequently (60-65 % of patients). The temperature increases till 38-39 °Ñ. The duration of the fever is 12-14 days. The signs of the intoxication are expressed temperate.

During the serious course of the epidemic typhus fever expressive intoxication, hypotonia, tachycardia (till 140 beats per minute) are observed. The tones of the heart are muffled. There is acrocyanosis. The dyspnea occurs, it may be violation of the rhythm of the breathing. The cramps of the muscles, the-violation of the swallowing are marked. The temperature increases up to 40-41 °Ñ. The rash is petechial, it may be hemorrhage. The serious course occurs in 10-15 % patients. The serious and very serious course of the disease takes place in elderly people.

Complications

Bronchitis, pneumonia, otitis media, parotitis, nephritis, tromboses of various vessels,both abdominal and peripheral may occur.

D

. mgnosis

In the proper setting of cold weather, infrequent bathing and changing clothes, crowded conditions, and the presence of lice, the clinical symptomatology described before is compelling evidence for the presence of louse-borne typhus. The progression of rash serves to distinguish the disease from Rocky Mountain spotted fever (RMSF), which progresses centripetally, beginning on the wrists and ankles. Diagnosis requires a high index of suspicion because of the great variability in presenting symptoms. It is important to examine the axillary folds

repeatedly for evidence of rash. During the colder months of November throq March, if RMSF is suspected from the clinical picture, tt should be a clue in considering the diagnosis of epidenj typhus. The Weil-Felix reaction is the same as in murine typhus; special serologic methods are used to differentiate louse-borne typhus from murine typhus. The polymerase chain reaction may provide an full alternative to serodiagnosis or rickettsia cultivation.

The methods of the laboratory diagnostic are serological: indirect hemagglutination, indirect immunofluorescence, complement fixation.

Differential diagnosis

Nonrickettsial infections at some time during the course, may mimic louse-borne typhus include meningococcemia, measles, typhoid fever, bacterial meningitis, secondary syphilis, leptospirosis, relapsing fever, infectious mononucleosis, and rubella.

During the period of onset of the diseasethe differential diagnosis is performed with grippe,pneumonia,meningitis,hemorrhagic fevers. During the period of the

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climax the differential diagnosis is performed with typhoid fever, ornithosis, drug disease, leptospirosis, infectious mononucleosis, trichinellosis.

Treatment

Preparations of tetracyclines - tetracyclin, metacyclin, doxycyclin are most effective.

Laevomycetin, erythromicin has less expressed action. At serious course of disease infuse antibiotics in vein or in muscle. Course of treatment carry out during all period of fever and 2 days of normal body temperature.

With desintoxication purpose in vein infuse solution of glucose, solution of Ringer-loc, donor albumin, reopoliglyc, polyvitamin, ascorutin. At psychomotor exaltation and deliriums - aminasin, fenobarbital, sodium hydroxybutyrat, sibazon (seduxen); for rising a tone of cardiovascular system and disorders of circulation - cordiamin, coffein-sodii benzoat, sulfocamphocain, ephedrini hydrochlorid, corglykon or strophanthin are indicated. At rising of intracranial pressure and the phenomena of meningism dehydration with due to furosemid (lasix), mannit is administered, sinapismuses or pepper emplastrum on nape and thorax, gastrocnemius muscle, feet, simultaneously intensive desintoxicative therapy and correction of hydro-electrolytic structure of a blood are also effective. At serious and very serious current of typhus use glucocorticoid preparations, anticoagulants (heparin or derivatives of dicumarin).

Prophylaxis

Control of the human body louse and the conditions that foster its proliferation is the mainstay in preveting louse-borne typhus.

Typhus vaccine is prepared from formaldehyde-inactivated Rickettsia prowazekii grown in embryonated eggs. Typhus vaccination is suggested for special risk group.

BRILL-ZINSSER DISEASE

Brill-Zinsser disease occurs as a recrudescence of previous infection with Rickettsia prowazekii. It is endogenic relapse of epidemic typhus. Brill-Zinsser disease is characterized by sporadic morbidity in absence of louse.

In Brill-Zinsser disease the pathogenesis and morbid anatomy are similar to epidemic typhus, however the process is less expressive, because the concentration of Rickettsia prowazekii is similar in the blood. The course of Brill-Zinsser disease is more mild than epidemic typhus, but the patients have all typical symptoms of the disease.

Initial period (it's duration is 3-4 days) is accompanied by temperate intoxication. Headache, disorder of sleep, increase of the temperature up to 38-39 °Ñ are marked. Enanthema is observed rarely (in 20 % of the cases). The duration period is usually 5-7 days. It is characterised by temperate hyperthermia (38-39 °Ñ) of remittent or rarely constant type.

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The signs of the damage of the central nervous system are expressed temperately. Meningeal signs are revealed rarely.

A rash is observed in 60-80 % of the patients. The signs of the damage of the cardiovascular system are marked frequently. Enlarged liver and spleen are revealed inconstantly.

In Brill-Zinsser disease the complications develop rarely. It may be pneumonia,

thrombosis, thrombophlebitis.

The treatment is similar to epidemic typhus.

The differentiation of primary louse-borne typhus is made by showing that the antibody produced is IgM (primary louse-borne) or IgG (Brill-Zinsser disease).

ENDEMIC TYPHUS (MURINE TYPHUS)

Murine typhus is widely distributed throughout many parts of the world. It has been encountered in the southeastern United States, South America, Syria, Greece,Africa,China and the Philippines.

Historic reference

Epidemic typhus fever was identified with epidemic typhus fever and other rickettsioses for a long time. It was described as independent disease by T.Hone (1922). The agent of the disease was isolated by M.H. Neil (1917). H. Mooser (1922) discovered rickettsia-like inclusions in the mesothelial cells of quinea-pigs infected by patient's blood. In Baltimore, Dyer, Rumreich, Badler (1931) isolated rickettsiae from the brain of rats and from rat fleas. In the same year H. Mooser, M.R. Castanedia, H. Zinsser isolated rickettsial from the brain of rats during epidemic in Mexico.

Etiology

The etiologic agent of murine typhus is Rickettsia mooseri, an obligate intracellular organism that shares common soluble antigens with Rickettsia prowa-zekii. The organism is less pleomorphic than R. prowazekii is; mostly cocco-bacillary form can be seen in cytoplasm on infected cells when using Giemsa stain.

Epidemiology

Murine typhus is zoonotic rickettsiosis. The disease occurs in those people whose occupation or living conditions brings them into close contact with rats and therefore the ectoparasites of these rodents. The rat flea Xenopsylla cheopis is the primary vector that causes human infection. Illness in human is a peripheral occurrence to the natural transmission of the organism in rodents.

Worldwide outbreaks and sporadic disease occur where conditions favor the proliferation of rats and where inadequate ectoparasite control exists.

In the rat, the disease is nonfatal. It is transmitted rat to rat by the tat flea and possibly by the rat louse. In the flea,the organism multiplies in the cells of

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the digestive tract without harm to the insect. Rickettsia mooseri is now thought to be transmitted transovarially in the flea.

When the flea takes a blood meal, it defecates. Its feces is heavily contaminated with organisms and produces infection in humans by soiling the bite wound. Infection may also occur by mucous membrane (conjunctivae or nasal mucosa) contamination with flea feces or by aerosol in laboratory personnel.

Pathogenesis

It is similar to epidemic typhus fever, but the pathologic process is less intensive. The destructive and thrombotic changes in the vessels and knotty changes in the brain are less expressed. The intoxication is temperate. There is an allergic factor of the disease. Its manifestations are the papular rash, damage of the joints of the hands and legs.

³

Anatomic pathology

The discription of murine typhus are pure because disease is rarely fatal. Necropsy showed intestinal pneumonia, alveolar hemorrhages, cerebral petechial, interstitial myocarditis, nephritis, splenomegaly. R. mooseri was demonstrated in the lungs, brain, kidney, liver, and heart. The histopathologic features that are described show the fatal illness to be quite similar to louse - borne typhus.

Rickettsia mooseri produces vasculitis by infecting the endothelial cells of capillaries, small arteries and veins. The process results in fibrin and platelet deposition and then occlusion of the vessel. Perivascular infiltration with lymphocytes, plasma cells, histiocytes and polymorphonuclear leukocytes occurs with or without frank necrosis of the vessels. The angiitis is most marked in the skin, heart, central nervous system, skeletal muscle and kidneys. If local thrombosis is extensive, gangrene of skin and/or distal portions of the extremities occurs.

Clinical manifestations

After an incubation period of 1-2 weeks, the disease begins abruptly without prodromal signs and manifests like epidemic typhus fever. Frequently^ nonproductive cough occurs early in the course. Although the illness is infrequently prostrating, patients are nonetheless unable to work because of headache and myalgia.

Rash occurs in 60-80 % of the patients, and it first becomes evident on the third to fifth day of illness. The rash is initially macular and occurs on the upper thorax and abdomen, and it remains central in distribution. This distribution is quite distinct from the primarily peripheral (ankles,wrists and face) distribution of spotted fever. Later, the rash of murine typhus becomes maculopapular and remains for 4-8 days. The rash may vary greatly in duration and intensity, and it may be quite evanescent.

In the untreated adult, temperature between 38.9 °Ñ and 40 °Ñ usually lasts 12-16 days. With antirickettsial.antimicrobial therapy, the temperature defervesces in 2-3 days. In either situation, convalescence is rapid. The disease is very mild

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in -young children. The disorders of the cardiovascular system are expressed temperatly. Usually the pulse corresponds to the temperature. It may be bradycardia. There is a tendency to hypotonia. The tones of the heats are muffled. Sometimes it may be a systolic murmur on the apex of the heart. It is manifestation of the infectious myocarditis. The changes in the lungs are observed rarely. It may be pneumonia or bronchitis. The liver is increased in 30-50 % of cases, the spleen is increased in 50 % of patients. The disorders of the central nervous system are less expressed than in epidemic typhus fever: The meningeal signs are absent. There are no typical changes of the blood. In the serious course it may be leukocytosis.

Complications

The complications occur rarely. It may be thrombophlebitis, pneumonia, otitis. The manifestation of the infectious myocarditis may also be present.

Diagnosis

The methods of diagnostics of the murine typhus are serological (complement fixation tests can be used for diagnosis).

In diagnostics of endemic typhus it is necessary to allow for similarity its some forms of the course with epidemic typhus (serious forms), Brill-Zinsser disease (medium serious and light forms) and other rickettsioses (Marseilles fever, Rocky Mountain spotted fever). In these cases gomologic diagnosticums are used. In abcence of differences biological tests is used for revealation of Nale-Mooser's scrotal phenomenon in males of white rats or quinea-pigs on 1-4 day after infecting by patient's blood.

Differential diagnosis

The differential diagnosis of murine typhus is quite complicated because of its usually nonspecific presentation. Aside from the rickettsioses and ehrlichiosis, alternative diagnoses that may need to be considered include meningococcemia, measles, typhoid fever, bacterial and viral meningitis, secondary syphilis, leptospirosis, toxic shock syndrome, and Kawasaki disease.

Treatment

The preferred therapy for R. typhi infection is tetracycline, doxycycline or chloramphenicol. Recent clinical trials of fluoroquinolones in the treatment of spotted fever group rickettsioses have been performed in Europe; the results of these trials and individual case reports suggest that such drugs including ciprofloxacin, ofloxacin, and pefloxacin may be effective alternatives. Whether such results may be extrapolated for broad treatment of R. typhi infection awaits additional studies. The current recommendation for tetracycline is 25-50 mg/kg/day in four divided oral doses, and for doxycycline, 100 mg is recommended. Chloramphenicol is effective when used at 50-75 mg/kg/day in

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four divided oral doses. In severely ill patients, intravenous therapy may be required,and doxycycline or chloramphenicol is preferable for patients in renal failure. Corticosteroids are occasionally used for severe CNS disease, but no controlled study to evaluate efficacy has been performed. Infected pregnant patients must be evaluated individually and either chloramphenicol (early trimester) or doxycycline (late trimester) may be used if necessary. Single dose therapy is not advocated since relapse may occur, and antimicrobial therapy should be continued until 2-3 days after defervescence. After initiation of therapy, patients become afebrile at a median interval of 3 days.

Prophylaxis

The measures for prophylaxis of murine typhus are systemic extermination of rats and mousses,prevention of bringing rodents into ports by ship,guarding food-stuff from infecting by urine of rodents.

The patients with murine typhus are not dangerous for surrounding people. The hospitalization is not obligatory.

The extermination of the sources of the infection (rodents and their ectoparasites) is performed by means of deratization and disisection. Killed vaccine from rickettsia Mooser is used in case of wide spread of the infection.

Mortality is very uncommon in murine typhus. Recovery is complete.

MARSEILLES FEVER

This disease has been designated by many geographic names: Marseilles fever, Mediterranean spotted fever, Kenya tick typhus, South African tick bite fever, Israel tick typhus and Indian tick typhus.

Historic reference

Marseilles fever was first described by Connor and Bruch in 1910 in Tunis. Subsequently different French and Italian observers reported the existence of a disease in the Mediterranean regions, in Marseilles and among other districts in southern France, as well as in Italy, Portugal, Spain, Greece and Rumania. The disease was said to resemble the mild typhus reported by Brill but small black spots of linear appearance resembling insect bites were often reported. There was no history of lice infestation.

Etiology

The etiologic agent is Rickettsia conori. R. conori is a typical spotted fever group rickettsia, having more than 90 % DNA homology with Rickettsii. There are also cross-reactive protein, lypopolysacharide antigens and cross-protection antigens, shared among R. conori, R. sibirica and R. rickettsii. R. conori is an obligate intracellular and intranucleus agent. It has both toxical and hemolytic activity.

Rickettsiosis

Epidemiology

Marseilles fever is transmitted by the common dog tick, Rhipicephalus sanquineus.

V.Durand has shown that the dog constitutes the reservoir of the R. conori. Dogs have been shown to be susceptible to inoculation and their blood has been proved to be infective both for man and monkeys. R. conori is maintained transovarially in ticks and is transmitted to humans by tick bite. Cases occur mainly in warm months with the peak incidence in July, August, and September in many Mediterranean locations.

Pathogenesis

Pathogenesis is similar to rickettsioses of the group of epidemic typhus fever, but the changes of the vessels is less expressed. The primary affect ("black spot"), regional lymphadenopathy and allergic manifestations are typical. The primary affect is local inflammation of the skin on the place of the reproduction of rickettsial with necrosis in the center. The black crust appears on the 5-8 day till rising of the temperature.

Anatomic pathology

Dermal and epidermal necrosis and perivascular edema are the consequences of endothelial injury by R. conori. Necrosis of fatal cases reveal disseminated vascular infection and injury by R. conori including meningoencephalitis and vascular lesions in kidneys, lungs, gastrointestinal tract, liver, pancreas, heart, spleen, and skin.

Clinical manifestations

The primary affect ("black spot") is an early sign of the disease. The crust usually falls on 4-5 day of the normal temperature. The localization of the primary affect is the strips of the skin covering by clothes. It is revealed by difficulty, because the bite of the tick is painless. After the incubation period of 7 days, fever, myalgia, and headache characterize the onset of the disease. On the 2-4 day of the disease the rash appears on the abdomen and then by the chest and alone all the body, including palms and soles. The rash is maculopapular. There is no itch. The changes from the side of the internal organs are such as other rickettsioses. Often the spleen is enlarged, the liver is enlarged rarely. The meningeal syndrome is not typical. The leukopenia, lymphocytosis, the raising ESR is temperate.

Complications

The complications occur rarely. It may be thrombophlebitis, pneumonia.

Diagnosis

The methods of the laboratory diagnostics are serological (complement fixation and indirect hemagglutination, with antigen from Rickettsia conori).

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Differential diagnosis

The differential diagnosis need to be considered with other rickettsioses because Marseilles fever has usually nonspecific manifestations. Alternative diagnoses that may include meningococcemia, measles, typhoid fever, bacterial and viral meningitis, secondary syphilis, leptospirosis etc.

Treatment

The treatment is similar to the other rickettsioses.

Prophylaxis

In endemic areas prophylaxis includes obligatory registration of the dogs every year, the processing of the dogs and the places of the tick.

Date: 2014-12-21; view: 1181