Toxoplasmosis

from Wikipedia, the free encyclopedia
Classification according to ICD-10
B58 Toxoplasmosis
B58.0 + Toxoplasma eye disease
B58.1 + Toxoplasma hepatitis
B58.2 + Meningoencephalitis due to toxoplasma
B58.3 + Toxoplasmosis of the Lungs
B58.8 Toxoplasmosis with involvement of other organs
B58.9 Toxoplasmosis, unspecified
K77.0 * Liver diseases in infectious and parasitic diseases classified elsewhere
Hepatitis due to Toxoplasma gondii
H32.0 * Chorioretinitis in infectious and parasitic diseases classified elsewhere
G05.2 * Encephalitis, myelitis and encephalomyelitis in other infectious and parasitic diseases classified elsewhere
J17.3 Pneumonia in parasitic diseases
ICD-10 online (WHO version 2019)

The Toxoplasmosis is a common infectious disease that primarily cats attacks. The pathogen is the protozoan parasite and the only member of its genus Toxoplasma gondii , for which cats are the main host . The disease rarely causes clinical symptoms such as diarrhea in cats. Cats only excrete large quantities of eggs ( oocysts ) of the pathogen during the initial infection , and then they develop a mostly lifelong immunity.

All other mammals, including humans, serve as an optional intermediate host for the pathogen. Symptoms of disease can also occur with these, so toxoplasmosis is a zoonosis . Intermediate hosts can become infected either through ingestion of the oocysts transported by cats (e.g. when gardening through contaminated soil) or through developmental stages of the pathogen in other intermediate hosts (humans primarily through raw pork and sheep meat). The infection of the intermediate hosts is also mostly without clinical manifestations. The first infection of pregnant women is particularly problematic, as the pathogen can pass to the unborn child and cause severe fruit damage, as well as the infection of individuals with a disturbed immune system.

Toxoplasmosis was first recognized as a disease in 1939. The transferability of the pathogen from cats to humans, discovered in 1908 by Charles Nicolle and Louis Manceaux in the rodent Gundi , was clarified in the mid-1960s by William M. Hutchison , who in 1970 worked with Jørgen C. Siim den Robert -Chef Award Received.

In Germany, toxoplasmosis in domestic animals is subject to reporting under the Animal Health Act .

Infection cycle

Schematic representation of the infection cycle of Toxoplasma gondii .

The infection cycle in T. gondii can occur in three ways:

  1. Definitive host cycle
  2. Definitive-intermediate host cycle
  3. Intermediate host-intermediate host cycle

Definitive host cycle

In the final host-final host cycle, the pathogen is passed on without intermediate hosts. Infected cats excrete oocysts in the faeces, which are then sporulated into the environment. If another cat ingests these sporulated oocysts via the food route, the sporozoites in them are released in the intestine during digestion. These traverse the intestinal wall and reach other organs and tissues via the blood or lymph . Here it comes to an asexual reproduction with the formation of so-called trophozoites within cavities ( vacuoles ) within the body cells. The infected organism reacts with the formation of antibodies and cysts form . In these cysts a further, albeit much slower, asexual reproduction takes place. The developmental stage of the pathogen is now called sporozoite or bradyzoite . Around the 18th day after infection, some of these bradyzoites migrate back into the intestine. Here there is a further massive increase through endopolygeny ( schizogony ) and through gametogony . The latter form the oocysts that are excreted in the feces. The prepatency - i.e. the time from infection to excretion of the first oocysts - is around 18 to 40 days for this infection cycle.

Oocysts are usually only excreted in cats when they are first infected. Subsequently, an immunity develops that, even with renewed infection, no longer leads to a full development cycle. Cats infected for the first time, mostly young animals, can excrete up to a million oocysts per gram of feces. Sporulation occurs in the outside world within a few days. The sporulated oocysts are very resistant to external influences and can remain infectious in moist soil for up to two years.

Definitive-intermediate host cycle

One or more intermediate hosts are involved in the definitive-intermediate host cycle. Cats usually get infected by eating meat from the intermediate host, which contains tachyzoites or bradyzoites . If tachyzoites - the intracellular developmental stages before cyst formation - are ingested, development in the cat proceeds as in the definitive host-definitive cycle with a prepatency of 4 to 8 days. If the cat ingests bradyzoites, the development phase outside the intestine is omitted and schizo- and gametogony with the formation of oocysts immediately takes place in the intestinal epithelium. The prepatent period is then only 3 to 6 days.

In this cycle, infection of the intermediate host occurs through ingestion of food or water contaminated with sporulated oocysts from cats. The sporozoites are released in the intestine. These pierce the intestinal wall and settle in various organs, especially the central nervous system , the eyes and female genital organs . Asexual reproduction ( endodyogeny ) leads to tachyzoites and, after about 10 days, cysts, especially in the muscles, the heart and the brain. Thousands of bradyzoites are then found in the cysts, which can grow up to 300 µm in size.

Intermediate host-intermediate host cycle

The intermediate host-intermediate host cycle takes place without the participation of cats. However, cats can also serve as an intermediate host themselves, but this is of no importance for epidemiology. The intermediate host is infected in two ways:

  • the uptake of bradyzoites from other intermediate hosts as well
  • transmission from the mother to the unborn child via the placenta (diaplacental).

The intermediate host-intermediate host cycle plays at least as important a role in the spread of toxoplasmosis in humans and the pathogen in general as infection via sporocysts from cats. The uptake of the bradyzoites takes place primarily through the consumption of the muscles of infected intermediate hosts, in humans mainly raw pork and sheep meat. The bradyzoites are very resistant, they remain infectious for up to 3 weeks at refrigerator temperature. Only freezing (<−20 ° C) or temperatures above 70 ° C kill them. They can withstand temperatures of 50 ° C for about 20 minutes.

Toxoplasmosis in cats

As a rule, cats only go through toxoplasmosis once in their life, after which they develop a resilient immunity , which is refreshed again and again through constant renewed contact with the pathogen ( premunity ). These cats never excrete oocysts again. The extent to which the disease breaks out depends primarily on the type of infection. When infected with oocysts (definitive host-definitive host cycle), only about 16% of the animals become ill, whereas when infected with bradyzoites (definitive host-intermediate host cycle), up to 97% become ill.

Even with the first infection, the disease in older cats is usually subclinical, i.e. without any significant symptoms. During the intestinal phase of the pathogen, slight diarrhea, short-term fever and swelling of the lymph nodes can occur. During the phase of parasite development outside the intestine (tachyzoite phase), depending on the organ affected, coughing, breathing difficulties, diarrhea, jaundice and inflammation of the middle skin of the eye ( uveitis , iritis ), the heart muscles ( myocarditis ), the skeletal muscles ( myositis ) or the brain ( encephalitis) ) occur. Sudden deaths can occur in kittens.

Chronic toxoplasmosis only occurs in cats with immune disorders. It shows itself in the central nervous system symptoms such as gait disturbances or convulsions , gastrointestinal problems such as vomiting, diarrhea and emaciation or inflammation of the middle and inner eye skin ( chorioretinitis ).

The diagnosis can be made during the elimination phase by examining the feces for oocysts using a flotation technique. In addition, antibodies can be detected serologically in the blood using IFAT . It should be noted that the antibody detection only indicates contact with T. gondii , only increasing titers in a second blood sample after about two weeks speak for an initial infection .

For treatment sulfonamide - trimethoprim combinations or clindamycin used in uveitis and glucocorticoids . Oocyst excretion can be drastically reduced with antiparasitic drugs such as toltrazuril .

Spread and ways to interrupt the infection cycles

In Germany, depending on the investigation, 45 to 75% of domestic cats have antibodies against Toxoplasma gondii . However, this number only shows that the cats experienced an infection once in their life, and with it, shed oocysts. However, the latter generally only happens with the initial infection for a period of up to 21 days, depending on the immune status. Only about 1 to 2% of cats shed Toxoplasma oocysts, especially young animals that have been infected for the first time. Rodents are of particular importance for the infection of cats in the definitive host-intermediate host cycle, of which about 0.1 to 0.4% in Germany carry bradyzoites.

In order to prevent the infection of intermediate hosts, the entry of oocysts into the environment must be kept as low as possible. Cats should not have access to pig or sheep sheds (the meat from these animals is the most common source of infection for humans). Cat excrement should always be safely disposed of, at least for indoor cats this can be done. Spots in larger cat holdings should be cleaned regularly with steam jets; almost all commercially available disinfectants are ineffective against the oocysts.

The most important prophylactic measure for cats is the feeding of exclusively heated meat or meat that has been frozen for a longer period of time to interrupt the cycle of final host-intermediate host or the exclusive use of ready-made food, which in particular with indoor cats makes the risk of infection extremely low. In the case of free-roaming animals, however, the intake of rodents does not provide effective protection against infection.

Toxoplasmosis in humans

Cerebral toxoplasmosis: Histological and immunohistochemical detection of pseudocysts in a human brain biopsy.

The main features of toxoplasmosis in humans apply in principle to all mammals that can be considered as intermediate hosts for Toxoplasma gondii .

Seroconversion, i.e. the change from missing antibodies against Toxoplasma to positive antibody detection, is a good method of determining the frequency of infection in a population. In Europe, the seroconversion rate varies from 7% (Norway) to 50% (Germany). In the FRG most people become infected through the consumption of insufficiently heated pork (raw sausage, ground meat). Vegetarians are less likely to develop toxoplasmosis. The infections occur in all ages. In Germany, 20% between the ages of 18-29 years are seropositive and 77% of the 70-79 year olds.

The incubation period in humans is one to three weeks, and if the immune system is healthy , the infection is symptom-free and symptom-free for about 90% of those affected. If the disease progresses in stages, the spread can drag on for weeks or years. The pathogens remain enclosed in cysts in the organism . They burst at any time and thus get into the blood vessel system and lymph vessels . If the illness is overcome, immunity can be assumed.

Antibiotic therapy is indicated for people with prenatal toxoplasmosis of the newborn, ocular toxoplasmosis and active Toxoplasma infection in immunocompromised patients.

General signs of illness

The infection is mostly symptom-free in healthy people with an intact immune system . Symptoms such as a slight fever, swelling of the lymph nodes in the neck area, fatigue and headache and body aches occur rarely. The course of the disease is usually favorable and the infected person does not need treatment. In the event of an infection, antibodies are formed that prevent infection from occurring again later.

Changes in behavior / personality changes

When rodents were detected by Toxoplasma caused behavioral changes. Infected animals lose their fear of the odor of cats and no longer protect themselves from being eaten, which is beneficial to the life cycle of Toxoplasma. However, the studies on behavioral changes in rodents do not show a clear trend. Recent studies also suggest possible links between the infection and schizophrenia in humans. Some studies suggest that behavior changes also occur in humans. Infected men were more introverted, suspicious and willing to take risks, and were more inclined to disobey rules and ignore the opinions of others. Women with latent toxoplasmosis , on the other hand, were more open, more trusting, more concerned about their image and more rule-following than the uninfected control group. A study in Slovakia and the Czech Republic with around 36,500 participants found a connection between toxoplasmosis and sexual tendencies.

The decrease in brain mass in the cerebral cortex , which is often observed in patients with clinically manifest schizophrenia , apparently occurs almost exclusively in the case of simultaneous (latent) toxoplasmosis, and the data suggest that it can lead to the onset of the disease with a corresponding genetic predisposition. Even suicidal actions should in people with latent toxoplasmosis occur significantly more frequently than in the general population. A study with almost 500 participants found a statistical association between T. gondii exposure and anxiety disorders , but not with depression or post-traumatic stress disorder .

The reports on the increased proportions of seropositive patients with various neurological and psychiatric diseases do not necessarily mean a causal relationship between the Toxoplasma gondii infection and the disease. This is already evident from the fact that all diseases also occur in people who are seronegative. The ability of the pathogen to intervene in the host's dopamine signaling pathways is, however, an indication that T. gondii could be a contributing factor in these diseases.

Complications

The immune system of embryos and fetuses in the womb and in newborns after birth is not yet developed. The fetus and infant are dependent on maternal antibodies through the mother cake and breast milk . In fetuses and babies and also in people with a weakened immune system (e.g. AIDS patients), foci of inflammation can form in all organs, most frequently in the brain, and lead to additional symptoms such as changes in character, paralysis and seizures. Additional manifestations from toxoplasmosis can be pneumonia and meningitis . Therefore, drug treatment is usually necessary.

Infection during pregnancy

Antibodies build up in the blood of women who have had a toxoplasmosis infection. Therefore, they are usually immune to infection and there is little danger to the fetus . Although these women can get a secondary toxoplasmosis infection, there is little danger to the fetus here either. Mothers with high antibody titers give birth to more boys than girls. A blood test can determine if there are antibodies to toxoplasmas in the blood.

If the mother becomes ill for the first time in the first or second trimester of pregnancy, this can lead to considerable damage to the unborn child. The likelihood of childhood infection is

  • in the 1st trimester 15%,
  • in the 2nd trimester 45%,
  • in the 3rd trimester 65 to 70%.

In the first trimester, 70% of infected children develop congenital toxoplasmosis, which usually leads to miscarriage . In the second and third trimesters, 30 and 10% develop congenital toxoplasmosis, which in 75 and 90% develop into latent toxoplasmosis and lead to considerable impairment in the child (see below). The infected children can have epileptic seizures , cognitive impairments, damage to the liver , lungs , brain , eyes , heart muscle and meninges . A quarter of the children infected with Toxoplasma gondii before birth have intellectual disabilities , spasticity , epilepsy , hydrocephalus and calcifications of the cerebral vessels . The typical triad , consisting of water head , intracerebral calcification and chorioretinitis , is only pronounced in 2% of those affected.

therapy

Antibiotic therapy consists in the administration of pyrimethamine , also in combination with sulfadiazine and folinic acid . Even clindamycin and atovaquone are among the usable antimicrobial drugs.

Therapy during pregnancy

A proven infection in pregnancy should be treated. The earlier treatment is started, the lower the likelihood of harm to the child (damage reduction up to 60%).

Toxoplasmosis in immunosuppression and newborns

Combination therapy of toxoplasmosis in the immunocompromised
drug Daily dose
Pyrimethamine
sulfadiazine
folinic acid 		2 x 50 mg
4 x 1 g
15 mg
For sulfonamide intolerance:
pyrimethamine
clindamycin
folinic acid
2 × 50 mg
3 × 600 mg
15 mg

In immunosuppressed people (e.g. newborns , AIDS patients or patients after allogeneic stem cell transplantation ), toxoplasmosis leads to disease patterns that do not occur in people with an intact immune system. Cerebral toxoplasmosis, which can manifest itself in the form of large, space-consuming processes with corresponding neurological deficits, is particularly serious. Sometimes the diagnosis can be difficult, especially the differential diagnostic differentiation from CNS lymphomas , which also occur many times more in immunosuppressed people. The diagnosis can be confirmed by detecting the DNA of the pathogen in the CSF using the polymerase chain reaction (PCR) or direct brain biopsy . It is not uncommon for suspicion to be treated. Medicines of first choice are the combination of pyrimethamine + sulfadiazine (+ folinic acid to alleviate the side effects of sulfonamide ), or the combination of clindamycin + pyrimethamine (+ folinic acid) in the case of sulfonamide intolerance . Pyrimethamine is also effective in combination with macrolides such as azithromycin or clarithromycin . However, these combinations are not recommended in the treatment guidelines. The duration of therapy is at least 4 weeks. The decisive risk factor for the occurrence of toxoplasmosis is the number of T helper cells in the blood. If the helper cell count is below 200 / µl, prophylactic medication , e.g. B. operated with 960 mg cotrimoxazole 3 times a week ("primary prophylaxis"). If toxoplasmosis has already occurred, prophylaxis must also be carried out to avoid recurrence (“secondary prophylaxis”).

See also

literature

  • Regine Ribbeck, Steffen Rehbein: Helminth pants. In: Marian C. Horzinek u. a. (Ed.): Diseases of the cat. 4th edition. Enke-Verlag, Stuttgart 2005, ISBN 3-8304-1049-2 , pp. 207-226.
  • Marianne Abele-Horn: Antimicrobial Therapy. Decision support for the treatment and prophylaxis of infectious diseases. With the collaboration of Werner Heinz, Hartwig Klinker, Johann Schurz and August Stich, 2nd, revised and expanded edition. Peter Wiehl, Marburg 2009, ISBN 978-3-927219-14-4 , pp. 234-237 and 294.

Web links

Wiktionary: Toxoplasmosis  - explanations of meanings, word origins, synonyms, translations

Individual evidence

  1. ↑ Karl Wurm, AM Walter: Infectious Diseases. In: Ludwig Heilmeyer (ed.): Textbook of internal medicine. Springer-Verlag, Berlin / Göttingen / Heidelberg 1955; 2nd edition, ibid. 1961, pp. 9-223, here: pp. 172-174, especially p. 172.
  2. ↑ Werner Köhler : Infectious diseases. In: Werner E. Gerabek , Bernhard D. Haage, Gundolf Keil , Wolfgang Wegner (eds.): Enzyklopädie Medizingeschichte. De Gruyter, Berlin / New York 2005, ISBN 3-11-015714-4 , pp. 667-671; here: p. 671.
  3. ↑ Annex to Section 1 of the Ordinance on Notifiable Animal Diseases (TKrMeldpflV) in the version published on February 11, 2011 ( Federal Law Gazette I p. 252 ), last amended by Article 381 of the Ordinance of August 31, 2015 ( Federal Law Gazette I p. 1474 )
  4. ↑ Barbara Hinney, Anja Joachim: gastrointestinal parasites in dogs and cats. In: Small Animal Practice. 58, 2013, pp. 256-278.
  5. ↑ Florence Robert-Gangneux, Marie-Laure Dardé: Epidemiology of and diagnostic strategies for toxoplasmosis . In: Clinical Microbiology Reviews . tape 25 , no. 2 , 2012, ISSN  1098-6618 , p. 264–296 , doi : 10.1128 / CMR.05013-11 , PMID 22491772 , PMC 3346298 (free full text).
  6. ↑ a b Hendrik Wilking, Michael Thamm, Klaus Stark, Toni Aebischer, Frank Seeber: Prevalence, incidence estimations, and risk factors of Toxoplasma gondii infection in Germany: a representative, cross-sectional, serological study . In: Scientific Reports . tape 6 , March 3, 2016, ISSN  2045-2322 , p. 22551 , doi : 10.1038 / srep22551 , PMID 26936108 , PMC 4776094 (free full text).
  7. ↑ Marianne Abele-Horn (2009), p. 234.
  8. ↑ Vyas et al. a .: Behavioral changes induced by Toxoplasma infection of rodents are highly specific to aversion of cat odors. In: Proc Natl Acad Sci US A. 104 (15), 2007, pp. 6442-6447. PMID 17404235 (full text)
  9. ^ AR Worth, RC Andrew Thompson, AJ Lymbery: Reevaluating the evidence for Toxoplasma gondii-induced behavioral changes in rodents. In: Advances in parasitology. Volume 85, 2014, ISSN  0065-308X , pp. 109-142, doi: 10.1016 / B978-0-12-800182-0.00003-9 , PMID 24928181 (review).
  10. ↑ Toxoplasmosis
  11. ↑ Jaroslav Flegr1, Radim Kuba: The Relation of Toxoplasma Infection and Sexual Attraction to Fear, Danger, Pain, and Submissiveness In: Journal of Evolutionary Psychology Volltext (PDF) 2016
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  13. ↑ Y. Zhang, L. Träskman-Bendz, S. Janelidze, P. Langenberg, A. Saleh, N. Constantine, O. Okusaga, C. Bay-Richter, L. Brundin, TT Postolache: Toxoplasma gondii immunoglobulin G antibodies and nonfatal suicidal self-directed violence. In: The Journal of clinical psychiatry. Volume 73, Number 8, August 2012, ISSN  1555-2101 , pp. 1069-1076, doi: 10.4088 / JCP.11m07532 , PMID 22938818 .
  14. ^ Marianne G. Pedersen, Preben Bo Mortensen u. a .: Toxoplasma gondii Infection and Self-directed Violence in Mothers. In: Archives of General Psychiatry. 69, 2012, doi: 10.1001 / archgenpsychiatry.2012.668 .
  15. ↑ Vinita J. Ling, David Lester et al. a .: Toxoplasma gondii Seropositivity and Suicide Rates in Women. In: The Journal of Nervous and Mental Disease. 199, 2011, pp. 440-444, doi: 10.1097 / NMD.0b013e318221416e . PMC 3128543 (free full text)
  16. ↑ Adam A. Markovitz, Amanda M. Simanek et al. a .: Toxoplasma gondii and anxiety disorders in a community-based sample. In: Brain, Behavior, and Immunity. 43, 2015, p. 192, doi: 10.1016 / j.bbi.2014.08.001 .
  17. ^ GA McConkey, HL Martin, GC Bristow, JP Webster: Toxoplasma gondii infection and behavior - location, location, location? In: The Journal of experimental biology. Volume 216, Pt 1 January 2013, ISSN  1477-9145 , pp. 113-119, doi: 10.1242 / jeb.074153 , PMID 23225873 , PMC 3515035 (free full text) (review).
  18. ↑ Š. Kaňková, J. Šulc, K. Nouzová, K. Fajfrlík, D. Frynta, J. Flegr: Women infected with parasite Toxoplasma have more sons. In: Natural Sciences. Volume 94, Issue 2, February 2007, pp. 122-127.
  19. ↑ Marianne Abele-Horn (2009), pp. 235–237.
  20. ^ A b Christian Hoffmann: Opportunistic Infections - Part 2: Cerebral Toxoplasmosis. (PDF 284 kB) HIV & more training, January 2008, accessed on May 28, 2011 (pdf).
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  22. ↑ a b Wolfgang Stille, Hans-Reinhard Brodt, Andreas H. Groll, Gudrun Just-Nübling: Antibiotic therapy: theory and practice of anti-infectious treatment. Chapter Toxoplasmosis in AIDS . 11th edition. Schattauer-Verlag, Stuttgart 2004, ISBN 3-7945-2160-9 .